There’s no doubt about it – L-form bacteria generate inflammation, and the eye is not spared from the actions of these persistent pathogens.

In many people who suffer from eye disease, the pigmented middle of the three concentric layers that make up an eye becomes inflamed. This condition is referred to as uveitis. Other parts of the eye can also become inflamed, causing conditions such as scleritis – a disease that affects the white outer coating of the eye. These conditions are both included in the umbrella name ocular inflammatory disease.

Many cases of ocular inflammatory disease are associated with “autoimmune diseases” like Crohn’s disease and rheumatic arthritis, or with illnesses of “unknown cause” such as Chronic Fatigue Syndrome and sarcoidosis – all of which have been recently linked to L-form bacteria. Thus, it comes as no surprise that these same cell wall deficient pathogens are also likely to be responsible for causing the vast majority of ocular inflammatory diseases. It’s also logical that people who have acquired enough L-form bacteria to develop one form of Th1 disease (and begin to suffer from decreased immune function) find that these same pathogens more easily infect other areas of the body, like the eye.

Other people infected with L-form bacteria develop “dry eye.” Many people with “dry eye” find that their eyes water but still feel dry. This occurs because the eye has two different tear ducts. Unfortunately, the ducts that produce tears necessary to maintain normal moisture in the eyes are often blocked or reduced by inflammation. Although the tears produced by the eye’s other ducts attempt to make up for loss of moisture, they do not have the same lubricating properties and simply cause the eye to water.

Normally, the conjunctiva, a membrane that covers the white part of the eye, is clear and white. Visibly red veins of the eye are a sign of vasculitis – a condition in which the veins of the eye become inflamed. This condition is common in patients with Th1 disease, especially if Bartonella is involved,” says physician Dr. Greg Blaney. “Because it is in the eye, it is very obvious and disconcerting.”^[1]

Presbyopia is another eye condition that affects the proteins in the lens, making the lens harder and less elastic over the years. Changes also take place in the muscle fibers surrounding the lens. The eye has a harder time focusing up close because of the loss in elasticity. Again, it is very likely that inflammation generated by L-form bacteria is what causes the lens and surrounding muscle fibers to lose elasticity in patients with the condition.^[2]

Cell wall deficient bacteria have been detected on multiple occasions in the eye. Researchers at Columbia under Emil Wirostko detected non-cultivable cell wall-deficient bacterial pathogens in patients with chronic ocular inflammatory disease. In one experiment, they injected these organisms into mouse eyelids, which subsequently caused the mice to develop inflammatory eye disease. They also found that these cell wall deficient pathogens could disseminate and cause similar inflammation in the heart, gut and lungs.^[3]

Similarly, Wirostko’s group noted that cataracts developed in the eyes of 14 of the 15 mice who had been exposed to the cell wall deficient forms, whereas no cataracts developed in the eyes of 200 control mice that had not come in contact with the pathogens. This data caused the team to suggest that cell wall deficient organisms can penetrate the lens capsule to produce cataracts, and that these same organisms could cause human cataracts.^[4]

Additionally, photographs by Emil Wirostko show a substantial number of L-form bacteria inside the immune system cells present in the vitreous of the eye. Several years later, his son, Dr. William Wirostko, implicated bacteria such as Staphylococcus hominis and Staphylococcus aureus in inflammatory diseases of the eye.^[5][6]

Similarly, researchers at the Massachusetts Eye and Ear Infirmary found Chlamydia pneumoniae present in the diseased eye tissue of five out of nine people with age-related macular degeneration (AMD) - a disease in which the center of the inner lining of the eye, known as the macula area of the retina, suffers thinning, atrophy, and in some cases bleeding. However, the bacterium was not found in the eyes of more than 20 individuals without AMD.

AMD can result in loss of central vision, which entails the inability to see fine details, to read, or to recognize faces. According to the American Academy of Ophthalmology, it is the leading cause of central vision loss (blindness) in the United States today for people over 50 years of age. “The paper showed that C. pneumoniae is capable of modifying the function of important cell types involved in regulating normal eye function,” said lead author Murat Kalayoglu, MD, PhD.^[7][8]

Bacteria in the eye cause the release of cytokines – proteins that cause pain and fatigue. These cytokines, which include TNF-alpha and interferon gamma, cause the tissues to become swollen and inflamed. The active vitamin D metabolite 1,25-D functions as both a hormone and a cytokine, and thus when increased, contributes to a rise in inflammation.

In patients with ocular inflammatory disease, the level of 1,25-D in the eye begins to rise for several reasons, all of which are related to the Vitamin D Receptor – a fundamental receptor of the body that transcribes a wide array of genes and enzymes. In healthy individuals, the Vitamin D Receptor transcribes an enzyme called CYP24. CYP24 breaks down excess 1,25-D, ensuring that the level of 1,25-D in the body stays in the normal range.

Unfortunately, as people accumulate L-form bacteria, the Vitamin D Receptor (VDR) is not able to function correctly. Molecular modeling has revealed that some bacteria are capable of creating substances that bind and block the Vitamin D Receptor - decreasing its activity.^[9] Vitamin D obtained through diet and excessive sunlight exposure (which is converted into 25-D) also has the same effect – meaning that once individuals have a sufficient load of bacteria in the eye and elsewhere in the body, the receptor can no longer transcribe CYP24. The level of 1,25-D in the body becomes significantly elevated since there is no CYP24 to keep it in check.

Another enzyme called CYP27B1 normally regulates the amount of 25-D converted into 1,25-D. When more CYP27B1 is produced, conversion occurs at a greater rate. In addition, the cytokines released by the immune system in response to L-form bacteria activate a protein called Protein Kinase A (PKA). PKA in turn activates CYP27B1, causing more 25-D to be converted to 1,25-D.

1,25-D and the retina

Many patients who suffer from these various forms of eye inflammation experience disturbed vision, which in many cases is due to the effects of elevated 1,25-D on the retina. The retina is a thin layer of cells that line the back of the eyeball.

The primary function of the retina is to act as host for the rhodopsins – cells that belong to the class of receptors that first sense light when it enters the eye. Rhodopsins commonly bind other molecules called retinals. When a molecule of retinal is bound into rhodopsin its shape will change if it is hit by a photon of light. The change in conformation causes a charge called an action potential to be conducted through the retina. When enough action potentials have accumulated so that a certain threshold is reached, a sensory signal is sent along the optic nerve to the brain.

According to molecular modeling research by Marshall, 1,25-D binds into rhodopsin, and will competitively displace retinal. Thus, as the presence of L-form bacteria in the eye causes 1,25-D to increase, the excess 1,25-D can directly interfere with the process of vision. “It is the high 1,25-D level due to intra-cellular bacteria which is the cause of abnormal optical phenomena,” says Marshall.

Additionally, the Vitamin D Receptor is involved in the transcription of several key proteins that form the structure of the retina

According to researchers at McGill University^[10] these proteins include:

• Epidermal retinal dehydrogenase
• Retinal outer segment membrane protein
• Retinal pigment epithelium-specific protein
• Retinal short chain dehydrogenase reductase
• Retinal outer segment membrane protein 1
• Retinal degeneration slow protein
• Arrestin 3, retinal
• Retinaldehyde binding protein 1

But as bacterial substances and 25-D bind and decrease the activity of the VDR it cannot correctly transcribe the above genes. Vision loss or foggy vision may result. “There are a number of retinal protein genes which are transcribed by the VDR, which is the reason eyesight fails as these Th1 diseases advance, and with advancing age. This provides another pathway for the Th1 bacteria to inhibit the proper operation of the eyes,” says Marshall.

The Marshall Protocol may help improve vision

Thus, people with inflammatory eye disease are able to use the Marshall Protocol to eliminate L-form bacteria, which are the ultimate cause of elevated 1,25-D. Patients take pulsed, low-dose antibiotics along with the ARB medication Benicar to active the innate immune system. With these measures in place, the patient’s own immune system can gradually work away at their bacterial load.

As patients on the Marshall Protocol begin to kill their L-form bacteria, the substances blocking the VDR decrease, and the inflammatory response of the immune system exacerbated by L-form bacterial death also slows. As the VDR regains the ability to transcribe the genes that form the eye’s retinal proteins, patients may experience improved vision.

It should be noted that some patients experience a drop in eye inflammation as soon as they start the ARB medication Benicar. This is because aside from its ability to stimulate the innate immune system, Benicar also has significant anti-inflammatory properties. Benicar binds and blocks the Angiotensin Receptor, decreasing levels of Nuclear Factor Kappa B, a protein that stimulates the release of inflammatory cytokines - causing a drop in inflammation. When researchers at the Keio University School of Medicine used a bacterial endotoxin to create a condition similar to uveitis in mice, they found that the eye inflammation of the animals decreased significantly after they were administered the ARB Telmisartan.^[11]

Of course once on the MP, patients should be prepared for changes in immunopathology – temporary rises in symptoms that result as the immune system deals with the increase in cytokines, 1,25-D, toxins, and cellular debri that are released when L-from bacteria die. This means that once on the MP, vision problems can be exacerbated in the short-term. Yet as more bacteria are killed and immunopathology dies down, these issues seem to resolve over time.

Case reports of Marshall Protocol patients noting improvement in vision and eye health are numerous.

“I was completely cured of severe uveitis by the very first stages of the Marshall Protocol,” says MP patient Julia Grier, who also suffered from floaters in the eye and elevated eye pressure. “In fact, I hadn’t even started the full MP with Benicar when my eyes began to heal quite dramatically, just on minocycline.”

Marshall Protocol patient Barbara Proal found that her corneal edema disappeared completely after only three weeks on the treatment. Before this point she had been forced to wear hard contact lenses in an attempt to help her blurred vision. Now her eyesight is clear and she can wear soft contacts again. “When my eye doctor saw that my corneal edema had resolved so quickly he was very impressed. In fact, I think he could hardly believe it,” says Barbara.

68-year-old MP patient Freddy Ash reports that since starting the Marshall Protocol his eye doctor has detected no inflammation, no granulomas, and no macular degeneration in his eyes. At a recent doctor visit he was told that the cataract in his right eye had not gotten any worse than the year before. Furthermore, the pressure in his eyes had decreased. “My eye doctor was well pleased with how the Marshall Protocol had helped my eyes,” says Freddie.

About 3 1/2 years ago, MP patient Leesa Shanahan developed swelling in her eyes. Within months her vision became fuzzy and her eyes painful, until she almost lost vision in one eye. Then, she started the MP. “From that moment on, my eye inflammation improved and I have not experienced one reoccurrence of uveitis in my eyes,” states Leesa. Before the MP Leesa was also forced to use large quantities of steroid eye drops along with oral medicines, steroids and methotrexate. Since starting the MP she has been able to wean off all meds and, at this point, no longer uses any of them.

Retinopathy, a condition in which blood has trouble reaching the eye is a common problem in patients with diabetes, but Marshall Protocol patient Debbie Y, who has suffered from type 1 diabetes for the past 46 years, reports that since starting the treatment, she has shown no signs of retinopathy. “My eye doctor even took photos of my retinas they were so perfect!” says Debbie. She also had psoriasis of both eyelids which after starting the MP is completely gone.

During a recent eye exam, Marie D’s opthamologist found absolutely no sign of cataracts in her eyes. “When asked if cataracts can be reversed, he responded with an unequivocable ‘no’,” states Marie. She found the response interesting because at her previous eye exam two years before (just as she began the MP), another doctor noted the start of cataracts, rating them 1 on a scale of 1 to 10.

“My eyesight is only getting stronger,” says MP patient Sue Andorn. For the last 50 years Sue has worn prescription lenses for farsightedness. She had a script change in May, and her prescription was not nearly as strong as it used to be. In fact, her current prescription is too strong. “My eye doctor can’t believe it. He was so impressed that he asked me for written permission to be able to tell his other customers about my progress on the MP,” says Sue.

“I had to start wearing reading glasses 7 years ago,” says MP patient Nicola deSousa “Every so often, I don’t need them - at all. These spells last about a day, but are fascinating because my vision is completely clear.”

The mother of a child using the MP to treat severe eye inflammation reports that at a recent ophthalmologist visit, her daughter’s right pupil, which had previously been irregular in shape was no longer so distorted. “The doctor says that she never would have expected the change,” says the mother. Furthermore, her daughter, who was previously taking high doses of the medication methotrexate, has been able to stop the drug completely. She has also significantly reduced the number of prednisone eye drops needed to keep her symptoms under control, yet her eye inflammation remains lower than it was pre-MP.

Another MP patient found that after about 8 months on MP, he was able to stop using the reading glasses that he had needed for almost 20 years. “My vision problems started when I got sick, and I had always wondered if the two were connected somehow,” says Sam. In fact he reports that after simply removing vitamin D from their diets, his wife and daughter have been able to stop using glasses. “My wife had reading glasses like I did, but my daughter had a script for distance vision. Pretty amazing stuff,” says Sam.

“I am reading without contacts,” says MP patient Sherry Cook. “I’m not sure my prescription has changed, but I don’t recall doing this for years.”

Similiarly, MP patient Gary Kays notes that about 10 years ago he started using glasses for reading and near-sightedness. However he’s noticed that after 3 1/2 years on the MP, objects in the far distance are actually clearer when he removes his glasses. He still needs correction for indoors and close use, and improvement is coming very slowly. He is quite happy that he no longer needs stronger reading glasses every year.

It should be noted though, that improved near vision may also be due to early cataract formation, which can begin as early as age 40. However, once the MP has brought inflammation under control, it is unlikely that a patient would develop cataracts.

Surgery

The above case reports, combined with molecular modeling data and other research on bacteria in the eye, strongly support the idea that the Marshall Protocol is able to lower eye inflammation in a curative manner – often eliminating the need for many extensive eye surgeries and palliative medications.

In cases where eye surgery is still necessary, the Marshall Protocol can still be used to lower inflammation in the time leading up to the event. “Every on-the-ball ophthalmologist would much prefer the patient to have very little to no eye inflammation at the time of eye surgery,” states the Marshall Protocol study site.

Unfortunately, the corticosteroid medications prednisone and prednisolone – which slow the activity of the immune system - can cause cataracts to form, meaning that the medications should be avoided. However, some patients on the Marshall Protocol have been forced to temporarily use steroid eye drops in order to manage flares in immunopathology. Experience has shown that they are usually able to wean off the drops over time.

MP patients can also use artificial (preferably preservative free) tear drops to manage immunopathology in the eye that temporarily brings back sensations of dryness. But patients should avoid drops that have ingredients for “red eye” or allergies as they may have immunosuppressive properties.

It’s also important for MP patients to understand that what may often feel like an allergic reaction in the eye is, in most cases, actually due to changes in immunopathology, meaning that no additional treatment is required.

Light sensitivity

The excess production of 1,25-D in the eye causes most people with eye inflammation and other Th1 conditions to become sensitive to light. As previously described, the elevated 1,25-D contributes to inflammation, particularly in the brain. As the levels of 1,25-D (which also functions as a hormone) rises, it also directly interferes with the regulation of the thyroid, stress and sex hormones – causing a rise in symptoms.

Consequently, patients with eye inflammation (and other Th1 conditions) must be careful about daylight and other light exposure. Many people find that just a few minutes of daylight aggravates their eye condition. Numerous anecdotal reports confirm the effects of increased and decreased light on the eyes of patients with Th1 inflammation.

According to the Marshall Protocol study site, “If the eyes are not adequately protected, the neurological symptoms can prevent tolerance of the immune system reactions and thus slow the progress of killing the bacteria. Exposure of the eyes to too much light will not prevent recovery but it will delay it and could make it a very rocky road.”

Thus, MP patients, particularly those with eye inflammation, are advised to wear special sunglasses made by the company Noir Medical in order to lower the amount of light that enters the eye. These glasses, which have an amber tint, block not only infrared rays, but also blue light and attenuate visible light in a manner that best blocks energy production.

The degree of light sensitivity that patients experience varies greatly from person to person for reasons yet to be fully elucidated - although in many cases, increased photosensitivity seems to be correlated with a higher bacterial load. Light sensitivity decreases as people progress through the MP, meaning once they have killed a substantial amount of bacteria, and the resulting inflammation they cause has decreased, it no longer poses a problem.

With these measures in place healing is possible - and in the end, few things are as valuable as the ability to see clearly. In this day and age, eye issues and blurry vision are considered to be a normal part of the aging process. But perhaps, thanks to the MP, most cases of impaired vision associated with inflammation and aging may prove to be a thing of the past.

REFERENCES

1. Buchanan, T. A., Harper, D. G., & Hoyt, W. F. (1982). Bilateral proptosis, dilatation of conjunctival veins, and papilloedema: a neuro-ophthalmological syndrome caused by arteriovenous malformation of the torcular herophili. The British journal of ophthalmology, 66(3), 186-9. [↩]
2. Wirostko, E., Johnson, L., & Wirostko, B. (1989). Sarcoidosis associated uveitis. Parasitization of vitreous leucocytes by mollicute-like organisms. Acta ophthalmologica, 67(4), 415-24. [↩]
3. Wirostko, E., Johnson, L. A., Wirostko, B. M., & Farris, R. L. (1993). Mycoplasma-like organisms and ophthalmic disease. Transactions of the American Ophthalmological Society, 91, 85-94; discussion 95-8. [↩]
4. Wirostko, E., Johnson, L., & Wirostko, B. (1991). Postinflammatory cataracts in the mouse: induction by human mycoplasma-like organisms. The British journal of ophthalmology, 75(11), 671-4. [↩]
5. Wirostko, E., Wirostko, W. J., & Wirostko, B. M. (2004). Age-related macular degeneration is an inflammatory disease possibly treatable with minocycline. Acta Ophthalmologica Scandinavica, 82(2), 243-244. [↩]
6. Iyer, M. N., Wirostko, W. J., Kim, S. H., & Simons, K. B. (2005). Staphylococcus hominis endophthalmitis associated with a capsular hypopyon. American journal of ophthalmology, 139(5), 930-2. [↩]
7. Kalayoglu, M. V., Bula, D., Arroyo, J., Gragoudas, E. S., D’Amico, D., Miller, J. W., et al. (2005). Identification of Chlamydia pneumoniae within human choroidal neovascular membranes secondary to age-related macular degeneration. Graefe’s archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv für klinische und experimentelle Ophthalmologie, 243(11), 1080-90. [↩]
8. Study Shows Bacterium Present In Eyes With ‘Wet’ Age-related Macular Degeneration. (2005). ScienceDaily. [↩]
9. Marshall, T. G. (2007). Bacterial Capnine Blocks Transcription of Human Antimicrobial Peptides. Nature Precedings. [↩]
10. Wang, T., Tavera-Mendoza, L. E., Laperriere, D., Libby, E., Burton MacLeod, N., Nagai, Y., et al. (2005). Large-Scale in Silico and Microarray-Based Identification of Direct 1,25-Dihydroxyvitamin D3 Target Genes. Mol Endocrinol, 19(11), 2685-2695. [↩]
11. Nagai, N., Oike, Y., Noda, K., Urano, T., Kubota, Y., Ozawa, Y., et al. (2005). Suppression of Ocular Inflammation in Endotoxin-Induced Uveitis by Blocking the Angiotensin II Type 1 Receptor. Invest. Ophthalmol. Vis. Sci., 46(8), 2925-2931. [↩]