Retinopathy is a disease of the retina of the eye where the blood vessels that supply blood to the matrix of photoreceptor rods and cones become damaged and occluded. This damage, in diabetic retinopathy, is directly caused by the underlying diabetes and hyperinsulinemia and related consequences of poor treatment, lack or treatment or of orthodox medical treatment. All three of these approaches amount to about the same thing, at least they all produce increasing loss of eyesight with blindness a predictable result.

The eye contains a matrix of arterioles, small arteries, and veins embedded in the material of the retina. When working correctly these veins and arteries provide a continuous blood supply that transports nutrient to all of the retinal  cells. These  cells, like all of the cells of our body, depend upon the blood stream to deliver oxygen and nutrients in order to perform their function. When these cells fail to receive this nutrition and oxygen  the body begins to try to compensate for the lack of it.

The reason that the oxygen and nutrition is not being delivered to the cells is two fold. First the small capillaries, or veins, begin  to leak. As we have noted earlier, the presence of chronically elevated glucose in the blood stream causes the small capillaries to become hyper-permeable; so they begin to leak. This leakage of blood, when near the surface of the retina, can be easily seen by an ophthalmologist when he  examines the eye with a ophthalmoscope. As they accumulate, these small patches of blood can and do form small blockages of vision. They seem like "floaters" or spots. When they become larger they actually block light from influencing our photoreceptors and we begin to experience a progressive form of blindness.

The small arterioles of the retina begin to experience atherosclerosis in exactly the same way the larger arteries of the body experience it. This causes a buildup of sclerotic plaque on their inner surfaces, and a stiffening of the wall with the consequent reduction of blood supply to the retina. If a blood clot, ischemic event, occurs in one of the larger arterioles or at a junction that supplies a larger part of the retina with oxygen and nutrition, blindness may occur as quickly as in a few hours. If a hemorrhagic event, sudden rupture of the arteriole occurs, the same thing may happen.

Both the venous leakage and the arteriole blockage are progressive. As the damage accumulates and vision becomes impaired the body, as always, tries to cope with the problem. In this case the way that it does so is to stimulate the growing of new arterioles and capillaries. This process is not all that effective. the new capillaries are more fragile than the old and soon become damaged by the chronically elevated  glucose and they too leak. The new arterioles also soon become occluded and blocked. This process of essentially trying to replace the circulatory system in  the retina is known as neovascular overgrowth.

Neovascular overgrowth is in itself a problem as it progresses. These new arterioles and capillaries position themselves so as to try to deliver the blood to needy parts of the retina. In doing so they form a tangled web of blood vessels that can and do interfere with the activity of the photoreceptors. They can also interfere with the activity of the optic nerve that transports digitally encoded visual information to the brain from receptors located on the retina.

This series of events, vascular leakage, progressive sclerosis of the arterioles and neovascular overgrowth can eventually cause structural damage such as retinal tears and retinal detachment.

Cataracts are another, but unrelated, consequence of untreated or ineffectively treated diabetes. Here  the problem is not with the vascular system of the eye but with the cells of the cornea. At the cellular level diabetic cells do not excrete sorbitol, a cellular waste product, efficiently. Sorbitol is an opaque substance that forms the appearance of the cataract. It is normally generated and excreted by all healthy cells during the normal course of metabolizing glucose.

As usual, orthodox treatment consists of attempting to deal with symptoms. If the patient is under treatment for diabetes he will typically be prescribed hypoglycemic agents to lower blood sugar. Virtually never will anything be done about the chronically elevated levels of other key hormones including insulin. He will be prescribed blood thinners and anti clotting agents in an effort to prevent an ischemic event. He will be prescribed hypertensive medication to lower blood pressure in an attempt to prevent a hemorrhagic event. Because the vascular system of the eye is responding to a systemic disorder the same way that the rest of the body is responding to the same disorder, is not at all unusual for this treatment to be prescribed because of the dangers of these events elsewhere in the body instead of just with the eye.

Since the invention of the laser, numerous ingenious ways have been devised to use it to make money in commercial applications. One of the worst is the widespread, almost standard, use of the laser to "treat" retinopathy. I have personal knowledge of the disastrous consequences of this practice. An acquaintance  of mine lost most of his eyesight as a result of laser treatment for diabetic retinopathy. The idea is to use the laser to burn and thereby scar the leaking capillaries. There are likely situations where this treatment is helpful to the patient. There are undoubtedly many situations where it  harms the patient unnecessarily and simply enriches the doctor for legally applying  an "approved protocol".

Since the leakage is progressive and the laser treatment is not, it cannot be said to prevent the leakage from occurring on any long term basis. There is even considerable question about its short term benefits. Furthermore, if, subsequently, the endocrine system is stabilized in the normal range by treating the underlying diabetes effectively, the capillaries will self repair very quickly without generating scar tissue. The sclerosis of the arterioles will also disappear and the neovascularization will cease. However, because of the scarring produced by the laser, the regeneration of underlying capillaries to form new healthy blood vessels will always be complicated by the presence of this scar tissue.

If the eye has already been damaged by laser treatment and subsequently the underlying diabetes issues have been effectively addressed, it may be possible to remove the scar tissue by the use of Serra Peptase and or Natto Kinase and similar polypeptide enzymes. These are digestive enzymes that digest protein. When taken between meals, instead of during or near meals, they are reputed to digest and remove unwanted protein from all corners of the body. If the eye has been damaged by laser surgery, this may very well be something that may help to remove the scar tissue and facilitate proper healing.

If the underlying cause of retinopathy is not effectively treated, blindness, along with many other terrible  consequences of diabetes, will usually ensue at some point.

Please go on to the next page in the sequence which describes hyperinsulinemia and Diabetes type II as the underlying causal agents of retinopathy More information is included in our special report, including a natural protocol which can readily arrest the progress of this disease in many cases.


1   Elaine  N. Marieb, R.N., PhD.; "Essentials of Human Anatomy and Physiology", fifth  edition. ISBN  0-8053-4185-4
    pp: 241-253  
2   William F. Ganong, M.D.,  "A review of Medical Physiology", nineteenth edition. ISBN 0-8385-8252-4  pp: 142-162
3  Robert Berkow MD, Editor, John H. Talbot, MD,Consulting  Editor, "The  Merck Manual of Diagnosis and Therapy"
    ISBN 911910-02-6  PP 1698-1714

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