Keratoconus | Eye Doctors Contact Lenses and New Options for Treatment

Keratoconus is an eye disease that causes vision to gradually worsen over time, as the transparent corneal tissue that covers the front of the eye thins and bulges forward, forming the cone shape that keratoconus is named for. Rapid increases in nearsightedness and astigmatism are common with frequent changes in your eyeglass prescription. Scarring of the cornea can also occur resulting in significant vision loss.

Keratoconus Symptoms Your Optometrist may discuss

• The appearance of long linear light streaks in your eyesight at night

• Visual Glare and halos around lights, especially car headlights and taillights at night

• Double Vision

• Distorted Vision

• Blurry Vision making it difficult to read

• Ghost like eye images of white light surrounding objects you are viewing, sometimes noticed as multiple dots when viewing on small light image-can be seen with one eye

• Eye Sensitivity to light

• Eye Doctors Agree Keratoconus usually show up most commonly between the teenage years of 16 up to age 30

When this corneal eye disease manifests at earlier ages optometrists often find a more aggressive form with ongoing, frequent changes in your eyeglass or contact lens prescription. The best guess is the occurrence rate is about 1 in 2000 people. It is hard for eye doctors to pin down the exact rate of this eye disease because it can be very mild and remain undiagnosed, especially when it burns out early (form fruste), or stops progressing after several years. Corneal Keratoconus creates irregular astigmatism, causing curvatures on the cornea tissue that are not nice smooth curves. Instead the eye curvature resembles the surface of a potato with dips and valleys on a very irregular shape. This type of shape makes it very difficult for your optometrist to prescribe an eye prescription for eyeglasses that results in clear vision. The lenses would have to be made in very strange shapes to result in clear vision. Even lenses that have been designed in this manner are rendered ineffective the moment your eyes look off the center of the lens. Irregular astigmatism also occurs without kerataconus, but it does not tend to progress and result in the characteristic steepening of the cornea resembling a cone shaped area. Usually kerataconus presents in one eye and over time well over half of the eye patients will have both eyes involved.

The cause of Kerataconus and the changes in the cornea are surprisingly not well known by the optometric research clinics at this time. In the past, much speculation centered around eye rubbing and ocular allergies. Some eye physicians have speculated that Keratoconus is triggered by eye rubbing that starts an inflammatory cascade in the cornea. Frequent eye rubbing also could cause mechanical tissue breakdown in areas of the cornea that are already compromised. Research by eye doctors has shown between 6-8% of patients with kerataconus have a family history, indicating there is a genetic component in some cases. Several areas of chromosomes have been identified as potential genetic markers and are being investigated further. Also, certain eye diseases such as retinitis pigmentosa, retinopathy of prematurely (damage to the retina tissue in the back of the eye from premature birth), Leber’s congenital amaurosis (a degenerative disease of the optic nerve), and vernal keratoconjunctivitis (a type of allergic eye disease which creates itchy eyes and frequent) appear to have some correlation. Some disease of the body also have a degree of co-occurrence with Keratoconus- Ehlers-Danlos syndrome, Down syndrome, osteogenesis imperfecta, pseuodoxanthoma elasticum), mitral valve prolapse in the heart, Laurence-Moon-Biedl syndrome, Rieger’s syndrome and neurofibromatosis. Several of these diseases interfere with normal collagen development and may precipitate kerataconus by disrupting collagen development in the cornea.

The changes to the cornea from Keratoconus are mostly unknown. The cornea consists of 5 layers and is about 1/2 mm thick (550 microns or about the width of 5 human hairs). The epithelium layer is the surface layers of cells. Underneath the eyes epithelium layers is a thin basement membrane sitting on the anterior limiting membrane, also know as bowman’s membrane. The bulk of the corneal thickness is in the stromal layer, where the collagen protein fibers run across the cornea, adding the tensile strength. Tensile strength is the degree a material can be stressed and still return to it’s original state and shape. Collagen is the memory material of the cornea. The structure of collagen changes in the center area of the cornea with shorter fibers, that cross more, run at different angles, run though each other, form connections to Bowmans membrane, and also form connections originating from Bowman’s membrane. It has been suggested from research by Jan P.G. Bergmanson, OD, PhD, PhD h.c, DSc, & Jessica H. Mathew, OD that this alteration in structure near the central cornea may help explain the nature of Keratoconus in the future, With shorter fibers running in differing directions with various connections the central cornea would seem to be more prone to breakdown of the normal collagen structure. Optometrists have found the bulging cone area characteristic of Keratoconus cones usually form close to the central cornea, slightly inferior, which seems to substantiate the altered central corneal tissues may play a part in the eye condition. Early changes may occur in the surface epithelial cells disrupting the basement membrane. When keratoconus begins, whatever the cause may be, enzymes increase and start damaging the epithelial basement membrane. This is the membrane formed underneath the lowest level of epithelial cells. Subsequent breaks in the corneal anterior limiting membrane occur and the cornea starts to thin centrally, probably due to the susceptibility of the different surface anatomy of the collagen fibers under lying Bowman’s membrane. As these breaks occur the surface epithelial cells can contact the stromal level of the cornea where most of the structural framework of this eye tissue is located. Small proteins called cytokines are released and alter the fluids around the cells, leading to scarring of the cornea.  Stromal fibers may move through the anterior limiting membrane. Whatever the cause, a disruption of the normal collagen structure causes the memory shape to lose its capacity and irregular shaped corneas to subsequently develop. There are indications of changes in the different enzymes that degrade proteins and induce changes in the collagen and the spaces surrounding the cells in the cornea. Cathepsins are one type of protein that increase as kerataconus starts to occur. These could lead to destruction of the so called extra cellular matrix, the substances surrounding the cells and lead to degenerative effects in the cornea.
They may also indirectly cause a reduction in the antioxidants and increase oxidative damage to the cornea, another theory that has been proposed. Matrix metalloproteinase-2 is also activated and changes the extra cellular matrix surrounding the corneal cells. Keratocytes are numerous cells in the cornea that produce the collagen for the fibers and the extracllular matrix components, turning mostly dormant by birth. In Keratoconus they have been observed to have increased apoptosis (increased programmed cellular death). There us a reduction in the number of collagen fiber and they also reduce in diameter. Most likely, keratoconus will be found to be several different disease processes and also multifactoral. Multifactoral eye diseases have multiple factors that combine to create the eye condition. For instance, the different collagen structure in the central cornea makes the eye susceptible, changes in enzymes may alter the tissues and start causing minor breakdowns in the epithelial surface cells, enzyme changes may lead to increased oxidative stress further weakening the eye tissue, and constant rubbing of the eyes may push the eyes over the edge by inducing mechanical damage to the eye tissues that could only occur with a compromised cornea. A genetic alteration of the cornea could make the cornea of the eye more susceptible to the entire chain of events.

Your eye doctor will initially treat Keratoconus with contact lenses

Treatment of Keratoconus usually begins with a rigid gas permeable contact lens when vision can no longer be maintained clearly with spectacle lenses. Sometimes, a gas permeable lens will be fit over the top of a soft contact lens in a piggyback contact lens fitting, with a soft contact lens and a rigid gas permeable contact lens on top of it. While used years ago, piggyback contact lens fittings fell out of favor due to the complications from reduced oxygen flow with older soft contact lenses. With the new super oxygen permeable silicone hydrogel soft contact lenses, it is enjoying a small resurgence. It is primarily used to increase eye comfort for the keratoconic eye patient. There are also combination contact lenses available today, such as the SynergEyes contact lens that is a rigid contact lens with a soft skirt attached surrounding the lens. The primary issue with Keratoconic contact lens fittings is matching the steeply curved cone with the surrounding flatter eye tissue, while dealing with the irregularities of curvature that are present. While custom mapping technology is highly touted as the way to achieve the required fit, the truth is observation of contact lenses on a keratoconic eye by an optometrist and adjustments based on how dyes accumulate under the contact lenses is still the most accurate method to achieve an excellent final fit. Due to the drastic changes in curvature the contact lenses require multiple different curves as you move toward the edge of the lens. While many different lenses have been developed with special names as the ultimate Keratoconus contact lens, they are all variations on the basic concept of a steep contact lens center and a gradient of changing curvatures to the edge. Rigid contact lenses work because the light bending capacity of the tears is very close to the light bending capacity of the cornea. The tears fill in between the irregular eye surface and the smooth surface on the back of the lens. This essentially removes the irregular astigmatism and nearsightedness by utilizing the back contact lens surface as a new regular surface where light is altered, and often restores the corrected eyesight close to 20/20. Eye glasses may only achieve 20/40 vision or much worse because the irregular surface remains. Occasionally Scleral rigid gas permeable lenses are used. These are gas permeable lenses larger than normal that extend out onto the white part of the eye. All contact lenses today are gas permeable, or designed to let air pass through to keep the cornea healthy. Soft contact lenses are usually not referred to as gas permeable because of historical changes. Hard lenses were the first contact lenses and they were made of a material that passed no oxygen through the lens. When changes were made to the polymers used to make hard contact lenses that allowed them to breathe or pass needed air to the underlying cornea, they were renamed rigid gas permeable contact lenses. Rigid because they are still a hard material with only 1-2% water, and gas permeable because unlike the older hard contact lenses they now transmitted air to the eyes. Soon they became called by the acronym of RGP’s to save a few words (even prior to the texting era). With time they also came to be referred to as gas perms, in spite of the fact that all soft contact lenses are also gas permeable. Soft contact lenses are never rigid however, as they normally are composed of about 50% water. This softness comes at the price of increased flexibility and they drape across the eye, imitating the irregularities of a Keratoconic cornea and do not correct the vision back to optimum levels. Once your eye doctor has achieved an excellent fit and optimized your contact lens prescription, there may be frequent changes in your contact lens prescription as the Keratoconus goes through progressive changes.

Your Eye Doctor May Be Able to Avoid Corneal Transplants

While only 10-20% of eyes will undergo ongoing serious changes, they do present challenges to fitting contact lenses on eyes with Keratoconus. At some point, scarring of the cornea can start to occur and patients become intolerant to contact lenses. In years past, the only remaining option was a corneal transplant. While corneal transplants enjoy a relatively high success rate, there are still risks and problems. Recently there have been some new exciting options starting to evolve.

Permanent Contact Lenses-Intacs

Intacs are small rigid half rings similar to portions of a gas permeable contact lens that are implanted in the cornea. They were originally developed to reverse nearsightedness, but did not prove as effective as originally thought and were replaced by LASIK eye correction procedures. A few years ago they found a new use in stabilizing Kerataconus. They are not a cure for Keratoconus, but can restore some more regularity and allow some patients to continue contact lens wear while avoiding a corneal transplant. They also appear to have some effect in decreasing the rate of change in Keratoconus. While they are promoted as being completely removable and reversible if patients have problems, this is not entirely true. About 10-15% of Intacs cause some complications and issues that cannot be resolved if they are removed. Still, it is a better option than jumping straight to a corneal transplant.

Keratoconus Corneal collagen cross-linking therapy

Corneal collagen cross-linking therapy (CXL) is intended to stabilize the tissue by forming more bonds between the existing collagen fibers and also increasing the size of the fibers, making the cornea much firmer and less likely to continue deforming. It involves pretreatment the cornea with riboflavin (Vitamin B2) for 30 minutes then using radiation from the ultraviolet A band light spectrum (normally around 370 nanometers) to increase the cross links over about a 30 minute period. While it has been more extensively in Europe, it is starting to enter the U.S. market. The riboflavin acts to keep the UVA from completely passing through the cornea so the UV can act to create more cross links. Riboflavin also may have a photo reactive effect that further increases cross linking of the collagen bands. Questions still surround this treatment. It is not an FDA approved treatment in the United States but is undergoing clinical trials, and currently is used off label as a treatment for Keratoconus. The FDA (Food and Drug Administration) regulates drugs and medical devices but not doctors. Any procedure that uses drugs or medical devices can be performed by a doctor if you are properly informed, share in the decision, and it has an acceptable possibility of helping. The riboflavin still allows a significant amount of UVA to pass through the cornea. This could potentially increase future risks for cataract development. UVA with riboflavin is cytotoxic (damaging to cells) and can damage the endothelial cells that line the back of the cornea and are vital for its long term health. Corneal thickness needs to be factored to keep this type of damage far enough away from the endothelium cells of the cornea. A minimum corneal thickness of 400 microns has been suggested but a better choice would be 450 to 500 microns. Cellular damage to the keratocytes, changes to the matrix of the cornea, and changes to the epithelium do occur in the cornea after the procedure. Normally they regenerate over the next 6 months. Riboflavin has poor penetration into the cornea so the surface layers of epithelium cells need to be removed. It is unknown if the effect of increased rigidity created by this treatment will last indefinitely, or if there are any other long term problems from increasing the cross linking and rigidity of the cornea. Some cases of persistent haze, infections, and increased eye pressure reading have been noted. The increased eye pressures are presumably an artifact since we know thicker (more firm) corneas read artificially high with most current glaucoma instruments. With careful consideration about the stage of Keratoconus and treatment of the eye at the appropriate stage, cross linking of collagen fibers in the cornea appears to be a great addition to eye doctors armetarium in treating keratoconus. While it may improve the condition mildly in many patients, it should always be considered as a stabilizing treatment and not a curative treatment.

Future therapies will evolve. Cross linking collagen therapy is still in its infancy. Stem cell and genetic treatments may be seen at some time. Someday we will no longer be treating Keratoconus but acting to prevent it from ever distorting peoples vision and lives.

SIX SIGNS YOU MAY HAVE GPC

FROM YOUR CONTACT LENSES

• Itchy eyes as contact lenses get older

• Lenses that slide and stick under the upper eye lid

• Irritation Every Time You Blink

• Mucous Discharge and Foggy Vision
  

• Lenses That Discolor and Develop a Film
  

• Intermittent Red Eye With Feeling Something is Scratching Your Eye
  

In the early years of soft contact lenses there was one choice, the Bausch & Lomb Soft Lens. The cost of a single pair of these miraculous new soft, comfortable lenses was between $300 and $400 when first introduced in 1971. Accounting for inflation, today that would be almost $2000. There was a very strong financial incentive to make the lenses last as long as possible. Using enzyme cleaners and sending lenses off for a special factory cleaning were common procedures. Lenses were often used for 3 to 4 years until they were yellowed and covered with numerous deposits from components of the tear film. Lipid bumps, calcium and mineral deposits, protein deposits and frequent tears and little missing chunks of the lens edges were tolerated well past the healthy tolerance of the eyes.

A new eye problem begin to show up in a number of the wearers of these new soft contact lenses. As lens technology progressed and prices came down lenses were replaced more frequently and the mystery red eye syndrome seemed to drop off. Then in 1981 the Hydrocurve soft contact lenses was introduced as the first contact lens for over night wear, the advent of extended wear contact lenses.  Cases of this new eye problem started to show up again and become common enough to recognize and diagnose.

The typical patient would come in to see the optometrist complaining about eyes that were red and irritated, possibly itching, and contact lenses that would slide around on the eye, sometimes falling out with blinking. On further questioning the lenses usually were sliding up as they would occasionally adhere to the underside of the upper eyelid. Frequently there would be some clear mucous or discharge from the eye, and some contact lens wearers would tell their eye doctor they kept seeing little spots on the surface of the lenses when they were handling them.

People have often admitted to me they turned their upper eyelids inside out as kids. For some unknown reason, girls more than boys, at least by admission. What was found in the 1980′s when inverting the upper eyelid is now referred to as Giant Papillary Conjunctivitis, or GPC. Usually it is referred to as GPC. There is a clear tissue that covers the white scleral part of your eye and extends underneath the eyelids as their surface lining. In GPC, giant papillae  (bumps of swollen tissue) form under the upper eyelid. These are described as giant but actually are about 1/3 millimeter in diameter. They do feel giant due to the highly sensitive nature of the clear tissue on the front of your eye, the cornea. Every blink rubs these bumps across the cornea and creates discomfort.

The cause of GPC has been disputed for years but most eye care providers agree there are two components, a mechanical irritation and an immunological reaction.

The lens edge constantly engages the underside of the eyelid with each blink that results in a form of low grade irritation and inflammatory reaction in a small percentage of contact lens wearers. There are probably multiple reasons such as how taunt or floppy the lid is, how the secretions make it more prone to slide over or stick to the lens, the variations in lid curvature that apply pressure to the lens at different areas, and if the conjunctiva tissue has a higher number of inflammatory mediators already present. Deposits on the lenses can also cause a mechanical type of reaction.

The immunological reaction is related to deposits that build up on the lenses. These can be your own tear lipids,proteins, preservatives in contact lens solutions that build up in the lens matrix, environmental allergens that build up on the lens, and in rare cases possibly the material the lens is made of. Since soft lenses are about half water they act like a sponge absorbing larger molecules and retaining them resulting in increasing levels over time.

Wearing the same pair of lenses for several years obviously caused an increase in this condition.  The hard lenses worn prior to soft contact lenses can still cause GPC, but because they are inert and do not absorb any water the incidence is very low. With the advent of extended wear, the eyes were given constant exposure to the mechanical and immunological irritants with no recovery time so the incidence started climbing again.

In the first era of contact lens technology lenses were frequently machined on a lathe when dry then re-hydrated. Bausch & Lomb developed spin casting the liquid material in a mold. Today automation and molding manufacturing techniques allow for much more precise and smooth lens edges. Lens that were hand inspected under a microscope in the past are now quality controlled by automated systems. These have been quantum  improvements in lens quality that have helped decrease lens edge induced GPC problems.  Extended wear contact lens materials are starting to be designed today to help resist deposits better.  For a number of years now the major contact lens manufacturers have been using large molecule preservatives that exceed the pore size of soft contact lenses. This greatly reduces the possibility of toxic preservatives inside the lens over time. Unfortunately, many generic solutions appear similar but often contain the older small molecule preservatives that can lead to GPC.

Even though the occurrence is much lower today, GPC can still be a major eye irritant and contact lens problem. There are several approaches to managing GPC. Switching to daily disposable lenses eliminates coating reactions completely since the lenses are thrown away daily and never exposed to disinfecting solutions. Usually, contact lens wearers with GPC have been wearing their contacts well beyond the suggested replacement cycle and become lax in cleaning the lenses. Returning to a normal 2-4 week replacement cycle and  discontinuing or decreasing overnight wear may be all that is required to return the eye to normal health.

Prescription eye drops are also a large part of treating GPC. A class of eye drops called mast cell stabilizers work to stabilize the cells membranes from releasing histamine that starts the inflammatory cycle. These eye drops are very safe and can be used year round when needed. Other options are available and today GPC is no longer the end of your contact lens career, only a small bump in the (eye) road.  Vision Insurance like Vision Service Plan Frequently offer plans that include medical treatment for conditions like GPC. You should do an annual review of all of your medical and vision coverage to make sure you are providing the best benefits you can for your family.

There is a new epidemic that is running rampant across the United States. Fortunately it is not contagious and not life threatening like the Swine Flu, but there is a tremendous cost in terms of loss of quality of life and vision. This epidemic is often referred to as Dry Eye Syndrome and effects millions of people with symptoms ranging from mild, vague discomfort to completely disabling pain and chronic blurred eyesight.The Dry Rye Epidemic has multiple causes.

• Time spent by adults on computers and youth on video games dramatically lowers the normal blink rate and causes the eyes to dry out faster than normal.
• Historically, before mass consumption of processed foods, for every unit of omega-3 fat we consumed in our diet we ate 1 to 4 units of omega 6. Today that ratio has shifted to 20-30 times more omega 6 fats in our diets than omega-3. This has caused an outbreak of disease of the eyelid margins and resultant poor tear film quality.
• As the population has aged there has been an increase due to normal, age related decreases in tear production.
• The large increase in prescription medication use has resulted in numerous drugs being used that contribute to dry eyes. Medications for blood pressure, depression, allergies, pain, and many other conditions can have drying effects.
• Millions of women treated with hormonal replacement therapy in the past may have increased the dry eye epidemic.
• With the shift to industrialized society, working indoors the patterns of airflow and humidity have been altered and effect the incidence of dry eyes.
• The long term shift away from water consumption towards caffeinated beverages and colas aggravates dry eyes in some individuals.
• Even the increase in obesity leads to low grade inflammation in the body which can decrease tear production.
• Many eyedrops, prescription and over the counter, can  cause or aggravate dry eyes to the point that some patients discontinue their treatment and suffer sight loss.
• Perhaps the worse culprit in the dry eye epidemic is LASIK eye surgery. The nerves that drive the eyes to blink are cut by the surgery and dryness is a frequent complaint after surgery. The dryness sometimes persists and requires long term treatment.

Fortunately we have many options today, including prescription eye  medications, new contact lens materials, glaucoma  eye drops designed for dry eyes, nutritional supplements, and even  micro-plugs implants for the tear ducts to help increase the basal level of moisture. If you feel you have symptoms of dry eyes please call and request an appointment for a dry eye evaluation. Your vision insurance service plan may provide coverage for dry eye treatment.

Symptoms could be any of the following:

1. Burning or stinging if the eyes
2. Eyes that intermittently water excessivley
3. Eye that feel griity at times
4. Vision that blurs up for brief periods of time
5. Pink or red eyes
6. Vision discomfort that gets worse as the day progresses
7. Developing intolerance to contact lenses
8. An increase in the normal level of itchy eye allergies
9. Frequent styes and eye infections

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Research on eye genes that cause or predispose individual to eye disease is a fast growing area which will probably find it’s way into your eye doctors office in the next 5-10 years. Most genetic tests are not perfect in the sense they are not diagnostic of an eye disease, but they frequently tell optometrists who may be more susceptible to acquiring the vision problem

in the first place, or which individuals may be prone to more severe forms.

Almost 500 genes have been identified that contribute to diseases of the eyes.  Mutations in the DNA  associated with a number of eye diseases, including glaucoma, cataracts, strabismus, corneal dystrophies different types of retinal degeneration. Diseases thought to be untreatable in the not to distant past are now being  targeted for future gene-based therapies.

Family members with relatives affected with genetic based eye diseases may want to know their risk factors and also for any future children. Unfortunately, testing is not readily available today, but the National Eye Institute is working to develop member labs to have this service  readily available at some point in the future.

The program initiated  to undertake this effort is referred to as the eyeGENE^TM program. It is a national progrma oordinating center, a centralized repository for blood/DNA/cell lines, several CLIA laboratories and a shared genotype / phenotype database. The goal of the NEI is to augment, not diminish, existing university-based and commercial ventures, while providing a new entry portal with rapid, reliable, and easy access to medical professionals.

Access to patient samples coupled to anonymous phenotypic data will augment the pace of ophthalmic genetics research, leading to improved medical decision making, clinical trials, and treatments for genetic eye diseases.

NASA and the National Eye Institute have been working together to develop a  non-invasive method to measure very early development of cataracts and monitor any progression. This is important to astronauts receiving higher daily dose of radiation, especially on a long mission such as the future Mars flight,  but there are great potential applications for preventing and treating cataracts in the future. The crystalline lens in the eye is composed largely of water but there is a class of  proteins present  known as alpha-crystallins.

The amount of  Alpha-crystallin Proteins in the eye are largely fixed at birth, we don’t produce more. They function to  a help the lens maintain it’s refractive index, which allows it to focus light on the retina so we can clearly see images. They also act as so called chaperone’s, dating the bad proteins that breakdown in the lens from oxidative stress. By joining up with theses proteins they prevent cross linking  between large numbers of damaged proteins and other damaged cellular substances that can develop into large clumps and form opacities in the lens. These capacities can develop large enough in size that they start to interfere with your eyesight and become clinically referred to as cataracts.

The new instrument measures how much Alpha-crystallin Proteins scatter light and can detect their levels and changes  over time. Now the potential exists to measure changes in response to environmental factors.

We have shown that this non-invasive technology that was developed for the space program can now be used to look at the early signs of protein damage due to oxidative stress, a key process involved in many medical conditions, including age-related cataract and diabetes, as well as neurodegenerative diseases such as Alzheimer’s and Parkinson’s," said NASA’s Dr. Ansari. "By understanding the role of protein changes in cataract formation, we can use the lens not just to look at eye disease, but also as a window into the whole body."

Oxidative Stress is caused by an imbalance between the production of Reactive oxygen species and your bodies capaictiy to neutrlaize them, the reactive intermediates, and repair any resultant cellular damage. Oxidative stress results from UV, radiation, drugs, chemicals,smoking, dietary components and other environmental factors that create oxygen is states where free electrons readily bind to cellular substances, Free radicals are atoms, molecules, or ions with unpaired electrons that also readily bind to proteins, lipids, and the DNA of our cells. When the threshold of repair is passed, and the Alpha-crystallin Proteins become lowered with age to the point where they can’t adequately act as chaperone’s to prevent these damgaed proteins from aggreagting into the clumps, you will likley develop cataracts.

Hopefully we can start to clarify some of the lingering questions and move forward into the arean of cataract prevention and reversal. Antioxidants have held out great hope for cataract prevention and anti-aging in general, but questions have been raised in some recent studies about the capacity of antioxidants to help.There is even a small school of thought that believes low doses of oxidative stress is essential in prolonging life. At this point, the only certainly is Vitamin A is contraindicated in smokers.

I still strongly believe in the value of antioxidants in a preventative role. Some studies have shown lutein and zeathin have reduced the incidence of cataract formation. Extensive studies are underway to test their role in treating macular degeneration. Vitamin C is still on my list as anti-catarogenic. One factor to keep in mind is natural is not always good. St John’s Wort does have some properties that my causes cataracts and sunglasses need to be worn and sunlight limited if you are taking St Johns Wort (commonly used for depression). This does not appear to be a strong causative factor but one to consider and compensate for when working in the sun.

Other lifestyle factors such as smoking, obesity, and eating a high glycemic index (highly refined high sugar,highly refined foods) are controllable risk factors. While I have not see the reasons published, presumably oxidative stress is the common factor. Smoking is know ot decrease antioxidants systemically  in your body, the cellular damage from free radicals is obvious in the loss of  skin elasticity. Even visible blue light causes oxidative damage in the retina and probably in the lens, Lutien and xeanthin may act as antioxidants in the lens to help prevent cataract development.

We can look forward to a great future in early detection (prior to visible damages) from cataracts and determining what lifestyle, dietary,and potential drugs ans supplements may prevent cataracts at some point in the future.

For now diet,exercise, a healthy body weight, a daily supplement (without the Vitamin A for smokers,  added Lutien, Zeanthin, and vitamin C is probably your best bet. And everything you can get from food (such as Lutein from spinach or other foods with high levels is presumably better than a pill.—Add protect your eyes from the UV sunlight with quality sunglasses or UV blocking contact lenses.

The next time you see your Eye Doctor they may just be measuring your alpha-crystallins levels, especially if you signed up for that 3 year cruise to Mars.

Our office is a Proud Participent in Vision Service Plan, and we work with you to maximize your understanding of  your vision insurance plans benefits. It is one more way of thankng you for entrusting your eye axam and vision care with us.

Fort Collins Optometrist

If you are doing a search for a local eye doctor in Fort Collins for your family please take a moment to look over our web site. You can find many answers to the questions you have about your families eye conditions, eye problems, and eye symptoms. If you don’t see an answer leave a comment and we will be try to find the information you request. We would like to have the opportunity to serve you family eyecare needs. We are a locaaly owned an operated eye care center serving Fort Collins and all of Northern Colorado. We will make your vision insurance claims as effortless as possible and accept most vision insurance plams including Vision Service Plan, EyeMed, Anthem, and most others. Please give us a call at:

970-226-0959

Welcome to Dr Kisling-Fort Collins Eye Doctors Choice Website. Our vision is to be the premier resource for answers about your eye symptoms and eye problems. You can use the search box to find answers to questions about your eyes. You will find articles on contact lenses, dry eyes, glaucoma, eye nutrition pinkeye ad other eye diseases.

There is also information about eye examinations, eyeglasses, prescription eye glasses for different conditions;nearsightedness,farsightedness, astigmatism, and presbyopia.

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If there is a topic you would like more information on please feel free to leave a request in the comment box. Thank you for visiting our website and we hope we can become your partner in preventative eyecare for a lifetime of healthy eyesight!

Melanocytes are specialized cells that contain the pigment found in our hair skin, eyes, and other area of the body. The eye has melanocytes in the iris, retina, and the choroidal layer under the retina that supplies it with blood. Underneath the retina is a layer of cells referred to as the retinal pigmented epithelium. These cells interact with the photoreceptor cells, the rods and cones that register light you see and turn it into electrical impulses. Melanin is the pigment and it comes in two different forms. In the retina, melanin acts as an antioxidant to help protect the tissue from free radicals that can damage the cellular DNA.

Various detrimental influences can reduce this protective function and may even cause it to accelerate damage from free radicals. Ultraviolet exposure, blue visible light, and high levels of oxidative stress can cause cell damage and increase the rate of cell death. An article by Meyskens FL, Farmer P, Fruehauf JP  suggested that this may be a contributory factor in macular degeneration and choroidal melanomas.

Melanocytes also populate our skin where they protect the underlying levels from ultraviolet damage. UV-B exposure is an essential step in producing the active form of  vitamin D. Darker skinned intervals have more UV screening and subsequently are more at risk for low levels of vitamin D. When you wear highly protective sunscreen the same effect occurs, lower levels of UV are absorbed by the skin and the proactive form of Vitamin D does not get its needed UV-B exposure to form. It is a very narrow band of UV-B that is needed, not the entire spectrum.

Vitamin D degeneration is related to multiple forms of cancer and other health problems. Macular degeneration may have an association with lowered vitamin D. One possibility is the overall reduction in UVB on the skin from sunscreen, living indoors, and poor dietary habits results in systemic changes in vitamin D levels that precipitates cellular changes in the retina unrelated to the melanin in the eye. Another possibility is lowered systemic levels of vitamin D resulting in decreased melanin production in the retina. This could lead to an overload to the pigmented epithelial cells from oxidative stress and UV exposure inside the eye, degrading the functional capacity of the melanin to protect the retina.
The irony is UV exposure is a risk factor for cataracts and macular degeneration and we are always encouraging eye protection against UV (and rightfully so given today’s evidence). With the known association of skin cancer and UV exposure it is not prudent to drop recommendation for sunscreen and limiting sun exposure.

At some point there will be better answers. For now, some mild daily exposure to UV with eyewear that includes UV protection is something you should discuss with your eye doctor and dermatologist or family physician. Vitamin D supplementation during winter months and in geographic locations that get limited sunlight should also be considered with your healthcare providers.  Perhaps sunscreen lotions will be developed that allow the narrow band of UV-B needed to pass through in the future.  Many people have vision insurance coverage like Vision Service Plan that provides coverage for eyeglasses. Even if your prescription is minor, having protection against UV and visible blue light is good preventative medicine if you spend time outdoors. And if you spend six months on a submarine or live underground you should examine your options-and maybe see a psychologist!

Reference:
Meyskens FL, Farmer P, Fruehauf JP (June 2001). “Redox regulation in human melanocytes and melanoma”. Pigment cell research / sponsored by the European Society for Pigment Cell Research and the International Pigment Cell Society 14 (3): 148-54. doi:10.1034/j.1600-0749.2001.140303.x. PMID 11434561.

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Glaucoma is a complex multi-factorial disease. In plain English, that means it is not one disease and not caused by one factor only. Recent knowledge has made us acutely aware that eye pressure is not the determining factor in the diagnosis of glaucoma. When the pressure inside the eye was above 21 in the past glaucoma was thought to be present. Today we know that some individuals will never develop glaucoma even though their eye pressure readings may stay in the 30′s while other patients cannot tolerate normal pressures without sustaining sight loss. Glaucoma is more of a vascular disease of the optic nerve of the eye. When the auto-regulation of the blood supply starts to fail, vision begins degrading. High eye pressures do cause compression of the blood vessels supplying the nerve, but healthy blood vessels with good autoregulatory mechanisms can sustain very high pressures. Eye pressure is not static and can vary throughout the day. When we read it once when we are at the optometrists office it is only a thin slice of what your pressure range could be over a 24 hour period.

The Human Genome Project mapped the human gene structure and was an enormous undertaking completed in 2003 taking 13 years and sequencing over 3 billion codes of base pair information. This has opened the doors to tremendous future strides in treating all diseases. There is a chromosome with a  gene that codes for the production of a protein called myocilin-a protein that makes up part of the  structure of the trabecular meshwork. This meshwork is responsible for keeping the fluid balance in check by allowing continual drainage. When something goes awry with the drainage the pressure goes up increasing your risk for developing glaucoma. Ocugene is a company that has developed a  test for defects in the myocilin/TIGR gene(GLC1A). Unfortunately, this gene is only responsible for about 4% of the cases of glaucoma. It can be useful when there is a suspected family history since patients with this genetic marker tend to have rapidly developing glaucoma and should be treated more aggressively. It also tends to be more commonly associated with glaucoma under the age of 40.The WDR36 (GLC1G) gene has also had mutations that appear to be associated with glaucoma. The optieurin gene(GLC1E) has reportedly been associated with an increased incidence of glaucoma in patients with normal pressures. One uncommon form of glaucoma know as exfoliation has also has seen the development of a genetic marker test, but due to the rarity of this condition it is not widely used .

All together, probably less than 10% of glaucoma has a direct genetic cause, and due to the expense of genetic testing it is rarely utilized. The complexity of testing is compounded by the fact that numerous defects at each gene can ocurr, and sometimes it may take two or more genes with flaws to create glaucoma. Even the most accepted genetic factor, the myocilin gene, may cause glaucoma from defects in areas other than the trabecular meshwork. It is very early in the age of genomics. Perhaps the greatest benefits will not be in diagnosing glaucoma but in tailoring treatment and actually curing some forms of glaucoma in the future.

General health issues are the most important risk factors, and some you can control. Smoking and cardiovascular diseases are high risk factors for developing glaucoma. Make sure you stay fit and have well controlled blood pressure. Keep preventative appointment and regular eye exams to monitor the eye pressure. Age is a risk factor but consider it a good one. A longer life is usually better all things considered! Most vision insurance plans  like Vision Service Plan, Medicare, and many others cover preventative annual eye examinations.

Twitchy eye? Many people become concerned when they start having an eyelid that twitches intermittently or even constantly. This may occur for weeks, months, or even years. Typically it does not occur constantly and has been coming and going for a month or so when the patient finally show up at the eye doctors office concerned they have acquired a serious vision problem. Most of the time after a lengthy eye exam and detailed analysis an accurate diagnosis is made-benign eye twitch. Essentially that means the doctor has no idea what is causing your eye problem but has ruled out  serious diseases

Sometimes a cause for eye twitching is found. Anything that causes ongoing low grade irritation of the eye can elicit twitches. An eyelash growing in towards the eye, dry eyes, a foreign body such as small particles of vegetation, insects, metal, etc. can all be provoke twitching eye lids. Some prescription medications and serious medical problems can precipitate eye twitches.

A well kept secret today is there are effective treatments for benign eyelid twitches. Specific types of topical antihistamine prescription eye drops frequently can alleviate the twitch, even though an eye allergy is usually not the cause. Reducing stress may help in many cases. Stress reductions techniques that help can include improving your sleep cycle by eliminating caffeine, relaxation techniques, and looking for areas to reduce the areas of high stress in your life. Cool packs on you eyes for 5-10 minutes several times per day can be tried as a palliative measure. Cold compresses probably reduce the nerve transmissions responsible for the eye twitching. If cool packs don’t work, warm packs sometimes will. Artificial non preserved tears can be used several times per day; they are not harmful and if a dry eye is part of the problem they could provide needed relief. Often a placebo effect can occur with artificial tears and is beneficial even when you are aware that it is a placebo.  Medications that can evoke eye twitches include stimulant drugs for attention deficient disorder, medications for Parkinson’s disease, some cold medications, and even asthma inhalers. If the problem is severe you should discuss your medications with your physician.

Some limited studies have shown complimentary alternative medicine may be useful is certain patients. Acupuncture has reportedly helped some people. Most simple eye twitches are probably similar to the twitches you have from time to time in you legs and arms. These are often due to muscle fatigue and electrolyte imbalances. Make sure you are well hydrated and have adequate magnesium, potassium, calcium, and vitamin D in your diet. Some healthy food to add are bananas, raisins, apricots, cantaloupes and leafy green vegetables like spinach. Avocado lovers can benefit also. Gentle stretching of leg muscle spasms has become the accepted standard replacing gentle massaging. You might try the eye equivalent of gentle stretching by slowly closing your eye, pause briefly, then open it slightly larger than normal and pause for a second. Try doing ten repetitions ten time per day.

When eye twitches become severe and spasm the eye closed it can be caused by an over stimulation of the brain center responsible for blinking. This has a genetic predisposition so if you have other family members with similar problems that is significant information you should tell your optometrist. Usually it begins with more frequent blinking and progresses to eye closure spasms. When eyelid twitches become constant and severe, they may keep the eye closed and interfere with vision. Injections of Botox, the face lifting drug, are a tremendous asset in these rare cases. Although many people are frightened by the though of injecting something into their eyelid that is so toxic it is considered a potential terrorist weapon, the doses used resemble homeopathy and are exceedingly safe. It would probably take at least 30 to 40 thousand doses at once to be lethal. Drugs in the same class as valium have had some success in treatment. As a last resort eyelid surgery can be attempted.

Uncontrollable, progressive eye spasms that effect you eye sight need further evaluation for serious underlying neurological diseases. The majority of cases are benign and the initial visit to an eye doctor can help you on the road to recovery.