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.
References:
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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