High frequency sex activity may lead to vision problems and eye disorders. If an orgasm induces excessive glutamate in the nervous synapse, photoreceptors or retinal extracellular space, an aging effect on the retinal circuitry will be observed.

Excessive sex induced stress hormones norepinephrine and epinephrine may damage retinal endothelial cells, inflame eye balls and retina, and dilate eye pupils.

There are several sex-induced eye or vision problems:

Eye Floaters

The deficiency of dopamine, serotonin, GABA, glycine, agmatine and androgen hormones (DHT, DHEA and testosterone) plus excess or deficiency of cortisol, norepinephrine, epinephrine and prolactin, may seriously damage visual sensor’s circuitry. The optometrists can’t detect quantities of them inside the eyeballs, steering the treatment to a wrong direction. Other symptoms may be present, such as: poor eye blood circulation, damaged eye capillaries, abnormal clearance of glutamate in certain photoreceptors in response to light, or even damaged photoreceptors that constantly release excessive glutamate to shut off the post-synaptic response to light.
When glycine (an inhibitory neurotransmitter in the central nervous system, brainstem, spinal cord, and retina) receptors are activated, chloride will enter the neuron via ionotropic receptors, causing the so called Inhibitory postsynaptic potential.


It’s caused by breakage of capillaries, inflammation by the excessive prostaglandin E2-norepinephrine-epinephrine and insufficient prostaglandin E1, mechanical damage, low cortisol, or excessive histamine.

Light over-sensitivity in the Retina
There is a circular opening located in the center of the iris that controls the amount of light that enters the eye. Excessive prostaglandin E2 (induced by excessive norepinephrine) and histamine in the retina, accompanied with lack of serotonin, glycine, GABA and prostaglandin E1, can over-excite the visual receiving sensors.

Melatonin is the main light sensitivity regulator. It is responsible for the photomechanical movement, cone photoreceptor and elongation and the contraction of different photoreceptors. Melatonin decreases when the light is decreasing, this is done to increase the photosensitivity of the receiving circuits, thus compensating the weak visibility by clearing the perception. Also, a dopamine is being released in the retina, but increases after light exposure and decreases in darkness. Melatonin is the darkness hormone while dopamine is the light hormone.

As a feedback control of the visual circuit, the photosensitivity of the receiving circuit decreases as dopamine increases, so that there is no truncation of visual signals entering the visual cortex. When the dopamine level is too low, though, the retinal receiving circuit becomes too sensitive to light. The eye pupils become dilated by the norepinephrine – sympathetic nervous function.

Melatonin also modulates the retinal pigment epithelium (RPE) function by aggregating pigmented cells in the RPE and choroid of the eye. Another way for melatonin to regulate the amount of light entering the photoreceptor is by controling the movement of melanosome granules within the RPE where melanosome granules store melanin. Melatonin can also alter the electrical activity of the RPE.

The darkness neurotransmitter is glutamate. It is modulated by the receiving circuit by decreases in its concentration. When we expose our eyes to light, it will take a while to turn on the color receiving circuit by removing glutamate. What is unfortunate is that dopamine and glutamate are essential to sexual arousal and orgasm. During sexual activity, the excessive glutamate turns into GABA, 5-HTP to serotonin, and the dopamine to norepinephrine. The result is an elevation of melatonin to suppress dopamine synthesis. In the more severe cases, the glutamate will not turn to GABA and the dopamine drops too low, leading to light-oversensitivity and eye floaters in the retina.

Blurred Vision and Central Serous Retinopathy

Numerous factors may contribute to these symptoms, such as:

  • Excessive prostaglandin E2 and insufficient prostaglandin E1 in the eye balls.
  • Excessive neuroexcitotoxic glutamate in the extracellular space of the retina, causing visual nervous damage
  • Excessive epinephrine in the eye balls or/and excessive sympathetic nervous action, which will dilate the eye pupils
  • Completely wrong eye balls chemistry – deficiency of DHEA, testosterone, DHT, excessive or insufficient cortisol and prolactin.
  • Abnormal levels of acetylcholine and dopamine in the visual sensing circuits
  • Acetylcholine deficiency or blockage, that will disrupt the retinal activities and visual signal output, leading to visual blackout, or even blindness.