 |
| Author | Post |
|---|
Meg Mangin R.N.
Research Team
|
Posted: Sat Sep 17th, 2005 02:33 |
|
Will immunopathology cause increased eye inflammation?
Immunopathology can increase eye inflammation even in folks with no history of eye inflammation. Various symptoms have been reported, including increased sensitivity to light, bloodshot (red) eyes, conjunctival bleeding, glazed vision, infection type symptoms and various visual disturbances. Vision exams may not reveal any abnormality.
Visual changes may also originate in the brain without organic change in the eyes. Eye muscles can also become weak as they heal. These eye symptoms could also be exacerbated by immunopathology.
Bacteria is the eyes
"I recently showed that 1,25-D directly activates the Rhodopsin receptors in the retina of the eye. These are the sensors for light. They work in a complicated fashion, so I won't attempt to explain it here, but it is the high 1,25-D level due to killing of the intra-cellular bacteria which is causing your optical phenomena, not the meds. OK, well, it is due to your taking the antibiotic meds, but only indirectly.
The retina of the eye sees a spot of light when a number of receptor molecules, rods or cones, are excited by photons of light. The Xray structure of the rods (Rhodopsin) is known. I have found that 1,25-D binds with high affinity into these. Most scientists seem to think that a cluster of about 5 need to be triggered by photons in order for the brain to see a spot of light. When 1,25-D levels are very high in the eye itself, then some of these rod receptors will always be excited, by the 1,25-D. One member has reported tiny white 'snow flake spots' in the darker parts of an image. The experience of 'glare' sounds similar. So do the more common "floaters." ..Trevor..
Dec 07 "The rod receptors in the eye are GPCR, similar to Angiotensin-II receptors. There is an Xray model available for Bovine Rhodopsin, and I used that to show that not only are the receptors activated by Retinal, but 1,25D has a high affinity for them too. I am guessing that the receptors are activated by 1,25-D (rather than de-activated), but we don't know enough about the eye to say that just yet.
It is believed that when a pool of about 5 adjacent receptors are simultaneously activated, the electrical signal so produced is sufficient to produce a pulse on the optic nerve. So sight is not based on a single receptor, but on a pool of adjacent receptors. When receptors are activated by 1,25-D (being formed in the eye by incident radiant energy), it will activate vision, but presumably by providing a continuous random stimulus. The optic nerve and brain then have to try and sort out where an image is, based on a consensus of false and true signals from the receptors in the retina.
Additionally, 1,25-D has the role of activating the VDR to produce several key proteins for the retina, without which the retina cannot remain strong and functional. The bacteria in the eye will obviously affect this process of transcription, which is probably why ocular symptoms (floaters, etc) are so common in these diseases." ..Trevor..
Managing immunopathology
The MP attempts to minimize the chance of eye damage due to increased inflammation by maintaining a tight Benicar blockade. Altering the antibiotic/s dose and scheduling can manage the severity of immunopathology by slowing the bacteria killing and thus reducing the chance of eye inflammation.
Infammation can damage the delicate structures of the eyer. Anyone with a history of eye inflammation, especially uveitis or iritis, should have their eyes examined regularly while on the Marshall Protocol. See Eye exams
Adequate eye protection will be particularly important for anyone with eye inflammation. Please see Protecting Your Eyes
See also:
Testimonials to the need to wear adequate eye protection
EYE INFLAMMATION and Th1 inflammation
Eye inflammation, vision, and bacteria
Light Sensitivity-basic information
Retinal detachment symptoms
|
Current time is 00:55 | |
|
|
|
|
