Theory of Sexual Orgasm: What is orgasm?

What is orgasm?
Dr. Lin has uncovered the mystery of sexual orgasm: The orgasmic expansion-contraction cycle of the smooth muscles and arteries is driven by the involuntary sympathetic motoring nerves under the alternative binding of norepinephrine and epinephrine into the sympathetic nervous adrenergic β- and α- receptors, as a result of the biological effects on the receptors exerted by oxytocin and prolactin, respectively. In other words, orgasm results from alternative activation of the α- and β- adrenergic receptors in response to the pulsing release of prolactin and oxytocin from the pituitary gland with an alternative cycle at 0.8 second.

Orgasm requires continuous erectile function of sex organs during sex. Erectile function dilates the arteries for more blood circulation and increases the androgen hormone (testosterone and dihydrotestosterone) and oxytocin stimulation on the neuromuscular endings in the sex organs, so that the nervous action potential generated by sexual stimulation can be amplified to jump above the critical synaptic potential threshold and can then reach the brain via the vagal, parasympathetic and sympathetic sensory nerves. Spontaneous erection of sex organs can be initiated by the cholinergic and parasympathetic nervous action which facilitate the secondary neurotransmitter NO (nitric oxide) release in the smoothing muscles of the arteries for the synthesis of vasodilator cGMP(cyclic guanosine monophosphate). The central cholinergic neurons can activate the hypothalamic oxytocin synthesis, and stimulate the anterior pituitary to release oxytocin into the bloodstream with a small portion of oxytocin crossing the blood-brain barrier back to the limbic and thalamic system for a positive feedback stimulation on the brain.
On the other hand, directly sexual stimulation via five sexual perceptions - hearing, sight, touching, smelling, and kissing, can also activate erectile function and sexual arousal via the dopaminergic, oxytocinergic, noradrenergic and sympathetic nervous pathway which are responsible for triggering orgasmic responses during sex. In addition to the directly sexual stimulation, sexual arousal and erectile function can be spontaneously induced by psychologically-induced dopaminergic action on the central nervous system in the limbic and hypothalamus, such as sexual fantasy, thought or imagination. Overall, the dopaminergic-driven sexual arousal generally promotes the hypothalamic dopamine-norepinephrine conversion with norepinephrine induced prostaglandin E2 in the brain and sex organs, essential to orgasmic responses. In some extreme cases, spontaneously sexual arousal can result in spontaneous orgasm without physical, sexual stimulation.
Upon sexual stimulation, the dopaminergic neurons in the nucleus accumbens and striatum are supposed to promote the pituitary oxytocin release (while reducing the prolactin release; otherwise, the sex organs going limp!), to fire up the oxytocinergic neurons, and, then, to initiate the hypothalamus and adrenal dopamine-norepinephrine-epinephrine conversion mechanism in the stress response axis - the hypothalamus-pituitary-adrenal axis for the noradrenergic, adrenergic, and sympathetic nervous activation. Noticeably, activation of adrenergic β receptors with epinephrine will facilitate the release of β-endorphin, which modulates the cellular sensitivity enhanced by norepinephrine-induced prostaglandin E2 and histamine in the alpha andrenergic receptors. Both prostaglandin E2 and histamine increase the nervous sensitivity, tissue erection and inflammation over the entire body, particularly in the brain, nipples, and sex organs, but they are also responsible for inflammatory pains in the brain and sex organs, sexual rushes, and premature ejaculation or orgasm. Obviously, the β-endorphin modulation on the nervous system becomes very critical for sexual pleasure and prolonging sex. Insterestingly, the central hypothalamic and adrenal norepinpehrine-enpehrine conversion seems to play an important role in stimulating β-endorphin release as noted in an experienment by repeated infusion of epinephrine http://www.ncbi.nlm.nih.gov/pubmed/2998913. It requires a threshold level of epinephrine to trigger β-endorphin release http://www.ncbi.nlm.nih.gov/pubmed/2532179 . The norepinpehrine-enpehrine conversion effeciency and the threshold level may depend on individual. Both alpha and beta adrenergic stimulation selectively release β-endorphin, but beta-adrenergic stimulation is more effectively. http://www.ncbi.nlm.nih.gov/pubmed/6283065. The beta-adrenergic stimulation causes the tissue expansion while the alpha-adrenergic stimulation results in tissue contration.
Further, the dilation of the brain arteries via the NOergic action and the noradrenergic action on adrenergic β receptors allows more oxytocin across the blood-brain barriers back into the hypothalamus and ventral tegmental area to increase extracellular dopamine release in the ventral tegmental area, supraoptic nucleus, nucleus accumbens and paraventricular nucleus in maintaining and prolonging dopaminergic action for sexual arousal. I have found that oxytocin elicits the binding of norepinephrine and epinephrine into the adrenergic β receptors to facilitate smooth-muscle expansion, arterial dilation, erectile function, libido enhancement, and testicular (ovarian) function by increasing the blood flow into the brain and sex organs, whereas its sister hormone prolactin promotes the binding of norepinephrine and epinephrine into the adrenergic alpha-(α-) receptors to facilitate smooth-muscle contraction, arterial constriction, limp erection, and ebbing libido. Interestingly, the opposite effects of oxytocin and prolactin on the adrenergic receptors form the orgasmic expansion-contraction cycle of the smooth muscles and arteries in response to the alternative oxytocin and prolactin pulsing release from the hypothalamus-pituitary axis. In other words, the orgasmic expansion-contraction cycle of the smooth muscles and arteries is driven by the involuntary sympathetic motoring nerves under the alternative binding of norepinephrine and epinephrine into the sympathetic nervous adrenergic β- and α- receptors, as a result of the biological effects on the receptors exerted by oxytocin and prolactin, respectively.
With orchestra effects of the cholinergic / (parasympathetic) and dopaminergic nervous action on the oxytocinergic and NOergic (Nitric Oxide neurons) system for the enhancement of arterial dilation and central oxytocin release, oxytocin and the enhanced blood flow continuously maintain stimulation of the testicular or ovarian function for continuous androstenedione, testosterone and DHT output which, in turn, fuel the dopaminergic nervous activation into the highest gear for heat in the brain and sex organs. This also results in an increase in the vaginal, clitoral and penile sensitivity and the prostate seminal fluid (or Skene's fluid) production. Once the dopaminergic, oxytoninergic, NOergic (Nitric Oxide neurons), cholinergic (vagal and parasympathetic neurons) and sympathetic nervous system (in its adrenergic beta receptors) maximize the sex-organ tissue expansion (strain) which produces an extreme stretching stress for the local neurons and induces an extreme prostaglandin E2 release to maximize the sensitivity of the neuromuscular endings in the sex organs at the same time, the hypothalamus-pituitary-adrenal axis in response to the extreme psychological and physiological conditions initiates an abrupt dopamine-norepinephrine conversion and drops the dopaminergic action on the pituitary function, leading to release prolactin for smooth-muscle contraction and arterial constriction to bring the blood out of sex organs in releasing the physical strain and its resulted nervous stress in the sex organs. After one-cycle contraction is over, the hypothalamus-pituitary axis releases the overproduced oxytocin to cause another smooth-muscle expansion again. Therefore, the expansion-contraction cycle repeats again and again. Gradually, the pituitary gland will release more prolactin but less oxytocin after each cycle. Eventually, the oxytocin-induced expansive and dilative effect on the arteries and smooth muscles will be suppressed by the contractive and constrictive effect of the accumulative prolactin in the bloodstream. At the final end of the expansion-contraction cycling, the smooth muscles return to the flaccid state, sexual arousal is over, and the oxytocin level in the bloodstream drops, but the prolactin level in the bloodstream reaches its peak. Each contraction of the sex organs sending a powerful action potential pulse to the heart, the lungs and the brain's rewarding center ( nucleus accumbens, the amygdala and the ventral tegmental area), pleasure center (prefrontal cortex), and conscious control center (cerebral cortex) via the vagal, sympathetic, parasympathetic and somatic sensory neurons is known as sexual orgasm. The period of orgasmic contraction cycle, that is the prolactin-oxytocin release cycle, is about 0.8-second based up our measurement of the orgasmic vocal responses. This is Dr.Lin's orgasmic theory. That is, the smooth muscles of the entire body, particularly in the heart, lungs, arteries and sex organs, will experience the 0.8-second expansion-contraction cycle during orgasm.
For men, the dominant orgasmic nervous pathway is the somatic and sympathetic sensory nerves, with a minor vagal sensory nervous transmission to the brain. This is because the sympathetic motoring nerves from Discs L1-L3 are responsible for the contraction of the prostate and seminal vesicles, leading to seminal ejaculation. In the prostate and seminal vesicles, the sensory nervous function and the sympathetic motoring nervous function are more active than the vagal and parasympathetic nerves. For this reason, men can suffer from involuntary ejaculation in the early morning or during watching pornography when the hypothalamic and adrenal dopamine-norepinephrine conversion becomes high enough to overpower the cholinergic, serotoninergic and GABAergic nervous control and modulation on the central noradrenergic and sympathetic nervous flow to the prostate and seminal vesicles, and to activate the sympathetic nervous contraction mechanism in the prostate and seminal vesicles via the binding of norepinephrine in the local adrenergic α- receptors to facilitate contractive ejaculation, even without muscle expansion. Men can feel a heat wave and electric pulse run along the spine and shoot into the brain in response to each orgasmic contraction, via the all sensory nervous inputs between the coccyx (Co) and the thoracic disc #12 (T12). This is why traditional Taoists consider the male sexual orgasm energy travels along the Governing Vessel (the energy channel in the central back body) of the acupuncture networks to the brain. Based up on my studies on the Chinese Tradition Medicine's Chi(Qi)-Blood theory, acupuncture channels are the most significant electromagnetic field lines jointly induced by the major nervous electric currents and the major blood (ion) flows in the body. The classical doctors didn't have any microscopes to discover neurons; instead, they were able to map the electromagnetic field lines over the body.

Theory of Sexual Orgasm

Saturday, December 19, 2015

What is orgasm?

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