Mild nonpriliferative diabetic retinopathy with  diabetic macular edema

With the numbers of people affected by both Type 1 and Type 2 Diabetes soaring in the US (an estimated 1 in 10 adults have diabetes currently in America, but that's expected to rise to 1 in 3 by 2050!), health care providers are actively looking for ways to not only treat this condition medically, but find ways to prevent the damage it causes to our body's most critical functions. The eyes are just one body part severely affected by uncontrolled blood sugar -- with diabetic retinopathy cited as the leading cause of blindness in American adults. Routine eye examinations are the best way to find early retinopathy during the stages before it has time to wreck vision; that's why your doctor takes retinal photographs and/or dilates the eyes every time you go in, even if you are seeing well that day. We know that better blood sugar control, exercise, and avoiding smoking can help reduce risks for diabetic related eye disease, but are there nutritional supplements that can be added to your diet to help protect your sight?  The Diabetes Visual Function Supplement Study investigated which nutritional additives could help protect your sight.  The study period was only 6 months in length with a small sample size (46 enrolled adults with both Type 1 and Type 2 diabetes were randomized between supplement and placebo groups).  But even over such a short reporting period, the results speak clearly about what else we can discuss with out patients for preventive care.

Science Behind the Nutrition

Lutein and Zeaxanthin: These carotenoids have proven essential to macular health, and are the most commonly recommended supplements for patients with sight threatening conditions like macular degeneration.  They are responsible for filtering out high energy blue wavelength light that can damage macular photoreceptors, and act as retinal tissue anti-oxidants.  Macular pigment optical density (MPOD) is the measurement of how much of these two carotenoids you have in your macula, and since your body cannot synthesize lutein or zeaxanthin by itself, diet is our sole method of intake. Studies show increased MPOD is linked to better visual acuity and contrast sensitivity in patients with nonproliferative diabetic retinopathy, and those with higher serum levels of lutein and zeaxanthin have a 66% lower risk of developing diabetic retinopathy.

Vitamin D: Vitamin D insufficiency has been linked to both the presence and the severity of diabetic retinopathy in both Type 1 and Type 2 patients.  And in fact, patients with lower vitamin D levels in general are much more likely to be diagnosed with diabetes, regardless of their body weight.  What role does vitamin D play in diabetes?  We don't fully understand exactly what the metabolic relationship is, but we do know that vitamin D appears to be vital to glucose metabolism and specifically in the eye can help regulate against neovascularization. Vitamin D can be absorbed through daily sunlight exposure, and also through dietary supplementation (milk is a great source!)

Curcumin (extracted from Tumeric): In animal models this supplement has proven to be protective against diabetic retinopathy, reducing inflammatory cytokine levels and neovascularization inducing VEGF.  A 4 week supplementation study in humans was associated with improved retinal blood flow, reduced retinal edema, and improved visual acuity in subjects.

Pycnogenol (pine bark extract): In a 3 month study, patients taking pycnogenol had statistically significant improvement in retinal edema, and blood flow through the central retinal artery compared to placebo.  Additionally 18 out of 24 patients in the treatment group experienced an improvement in visual acuity; none of the placebo group patients had visual improvement over the time of the study.

Benfotiamine (Vitamin B1 analog): This enzyme helps the body safely process harmful biproducts (sorbitol, protein kinase C, and others) of normal cellular glucose digestion.  In the retina, animal studies show it can prevent diabetic retinopathy, and it also helps prevent cellular death of the all important pericyte cells of retinal arteries (pericyte death causes the blood vessels to leak!).  It's also been shown to improve the symptoms of painful peripheral neuropathy in patients with reduced blood flow to their arms and legs.

Alpha Lipoic Acid: This is a potent antioxidant that targets mitochondrial cells (your body's cellular power house) -- a critical target because diabetic damage is linked to mitochondrial oxidative stress.  An 11 month dosage study in rat models showed that alpha lipoic acid was preventative against retinal vascular damage and the presence of diabetic retinopathy.

ZeaVision's EyePromise DVS formula via

Results of the Diabetes Visual Function Supplement Study

Compared to the placebo group, the supplement group had improved contrast sensitivity, less color vision perception errors, and lower C-reactive protein levels on blood work (a marker for systemic inflammation).  The supplemental group also had a 39% reduction in their Diabetic Neuropathy Symptom Score, a questionnaire that asks such questions as "does the patient experience numbness or tingling sensations in their feet or hands?"  There was also a minimal positive effect on hemoglobin A1C numbers for the supplemental treatment group -- with their mean A1C improving by 4% over the course of the study.  The placebo group's mean A1C worsened by 2.5% by comparison.

The supplement group showed statistically significant improvement in C-reactive protein levels after treatment (left) and increased macular pigment density and improved central visual field sensitivity (right) compared to the placebo group.  OCT measured macular thickness was unchanged in either group.  via

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While many will point out that this study was funded by ZeaVision, the company now marketing the EyePromise DVS supplement formulation investigated, the results when combined with the plethora of other studies on these individual nutrients are promising.  Discussing dietary changes or supplements in the exam room is definitely a worthwhile endeavor, but with any nutritional supplement it is always best to have the patient discuss any new medications (even vitamins) with their PCP to make sure there are no cross-interactions.  In an era where we are limited in treatment for patients in the early stages of retinal damage from diabetes, these studies suggest that dietary supplementation can not only help resolution of early nonproliferative diabetic retinopathy, but they can even improve visual ability and be preventative for further retinal damage!

You can order EyePromise DVS nutriotional supplements direct from ZeaVision here.

I am in no way affiliated with ZeaVision and this is a not a sponsored post!  Just a discussion of some really intriguing research.

Contact lens wear after 40 can be a challenge; today's multifocal contact lens designs often leave patients with compromised distance or near vision, or both.  The reason?  Multifocal contact lenses rely on a layered ring design, where rings of distance and near powers through the center of the contact lens create multiple images on the back of the eye that the brain must interpret.  The pattern and width of these rings is different with every contact lens brand design, which is why you can't expect to see the same out of Air Optix Multifocal as you do out of Freshday Multifocal.  One of the biggest limitations of this multiple ring design is that depending on the size of your pupil, you may get too much or not enough of each ring of vision.  And because these lenses are not custom made for your eyes, they either work or they don't -- there's no way to manipulate the ring design for your individual pupil.

We've all seen the startling numbers -- society as a whole is getting more and more myopic with each generation at a speed that can't be explained by genetics alone.  About 1/3 of the US population is near sighted, an increase of 66% since the 1970s, and in Asia the number of school children that are near sighted may be as high as 90%.  But with the World Health Organization now discussing a true myopia epidemic, scientists and researchers are struggling to understand in a very short time why our vision as a population is changing so rapidly.  The real truth is that we can only theorize what is causing our eyes to change -- studies on chicks and monkeys about how the eyes develop in different environments give us some insight, but to understand the human eye we often have to rely on correlational study data that can prove cause, only relationships.  The result is a number of theories for why myopia occurs and progresses:

Nearpoint Stress Model

Kids are drawn to visual stimuli like lights and colors, and they tend to like to get very close!  With the near point stress model of optometry, too much time or strain on the eyes this close may eventually result in us becoming myopic!  It gives credence to listening to mom and dad about not sitting so close to that TV. via

The most studied and discussed theory behind why children develop myopia is that it is a result of visual stress from near work.  Our eyes are evolutionarily made to excel at distance vision.  Images from about 20 feet away would have perfect resolution to details as small as 8.87 mm in size in a "perfect" or normal eye.  But today's world finds us even as very young children spending less time looking across the horizon, and more time looking at objects much closer.  Think about a book, cell phone, tablet, computer, television.  All of these items are much closer than what our eyes are theoretically best designed to see.   In order to see things clearly up close, our eyes use the focusing system (which includes the eye muscles and the lens inside the eye, also called accommodation) to bring focus closer in.   Our eyes are designed to be able to change this focus back and forth between distance and near until we age to the point that the system no longer works -- this is called presbyopia and it's why people can't see as well to read after age 40.  But in a young child, the focusing system is flexible and should be able to transition back and forth to see both up close and far away.  The near point stress model of myopia theorizes that if too much time is spent up close, or if for some reason up close work is more difficult than it should be, the eye will begin to change to reduce the amount of stress it has to overcome to focus clearly at near.  When the eyes design themselves for easier, clearer reading vision that means they no longer focus light clearly far away -- this is myopia.

Here's the body chemistry behind the model: our body responds to stress by activating the sympathetic nervous system.  You'll often hear this referred to as fight or flight.  When our body is stressed by environment or emotion or fatigue, or just about anything difficult or stressful, the sympathetic nervous system takes over.  This is the system that increases our heart rate, speeds up breathing, slows down digestion, and makes us more alert.  With the eyes, an activation of the sympathetic nervous system means that your pupils dilate so that you can take in more light and be more aware of your surroundings.  In order for your pupil to dilate, your ciliary muscle (the muscle around the iris that also controls our focusing system!) relaxes. As a side effect of this muscle relaxation, your focusing system relaxes.  Your body has entered an alert mode that was meant to help it see threats from far away --but that means you've just diminished the action of those eye muscles that let you focus on things up close.  So the theory here is that when you get stressed (you are learning to read and it's a hard word, you've been reading too long, you're tired), your body enters sympathetic/fight or flight stress mode and your body now makes it even harder for you to see what you are reading!  The result of all this stress? Your body has two choices: Fight (which can lead to common binocular vision issues like convergence disorders, accommodative spasm, and ultimately even the prescription changes that result in myopia) or Flight (which is what some children do -- they avoid reading, and may even get incorrectly diagnosed with ADD).

Need a refresher?  Accommodation is what each eye does to bring the image into focus clearly on the retina.  Convergence is the movement of the eyes together to point both eyes at the right place in space for clear focus on the image.  These two systems work in conjunction to keep vision clear and single. via

Let's say your body decides to fight -- what's going on in the eyes when they are fighting to stay focused up close?  When we are trying to focus on a near image but our accommodative system isn't able to handle the work to bring the image into focus, our eyes turn to the convergence system. Convergence is the system that brings the eyes together to focus on the same point in space.  When we look at something up close, our eye muscles turn in (convergence), and shift focus closer to the object (accommodation).  If you don't have enough accommodation to see clearly, then you draw more effort from the convergence system.  If you are over-converging to make up for insufficient accommodation, then your eyes have what's called an esophoric posture.  The problem? If you are overfocusing on a target, that means your eyes are much more likely to see double since they aren't positioned equally to where you are looking.  How do the eyes try to prevent from seeing double? They try to pull in more accommodation.  This back and forth balance between accommodation and convergence as they work to keep vision clear and single is called the AC/A ratio and one of the foundations of binocular vision system performance.  The theory of near point stress implies that accommodation and convergence are constantly out of balance in the patient at risk, and the eye adjusts its shape in order to relieve some of this constant pull and tug by becoming myopic.  Image can't focus clearly on the retina?  Well let's make that eyeball longer so that when I look up close the image falls on the retina without any effort from this beat up focusing system.  But if lengthening the eye is the body's way to solve the problem, why does the myopia keep getting worse?  The reason is that the balance of accommodation and convergence is still messed up, so the eye has to keep lengthening to keep things in check.

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In this theory, vision therapy may play a role in myopia control.  If we can find early children at risk -- children that have accommodation or vergence issues that are just starting to express themselves, then we can help the child develop their focusing system skills to handle the amount of near work required to get through the day at school and home.  If your doctor has talked to you about your child needing vision therapy or reading glasses or both, they may have mentioned something to the extent of "wearing glasses now may help keep them from needing glasses later."  If so, they are citing this near point stress concept of myopia progression.

Theoretically if nearpoint stress was the sole cause of myopia development, then wouldn't wearing bifocals that reduce the accommodative demand for near work prevent myopia progression?  Unfortunately this doesn't hold true in clinical research. Studies where children were prescribed single vision glasses compared to children prescribed progressive glasses (with a reading power in the bottom to reduce near accommodative demand) report no clinically significant reduction in how quickly myopia progressed.  Undercorrecting myopia has also been disproven as a possible means to slow myopia creep.  In fact, undercorrecting a child has been shown to make myopia progress faster than fully correcting the child's prescription! So if near point stress isn't the whole story, what else is causing myopia to develop in our children?  In our next post we talk the other two theories of myopia development: sunlight exposure and peripheral defocus theory.

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Whenever a new multifocal lens promises to deliver better visual performance, I am honestly skeptical.  The current daily disposable multifocal market had been rather uninspiring in lens technology with Proclear 1-Day Multifocal delivering relatively limited performance in higher adds (plus a fitting process that left a lot to be desired on initial lens selection) and the Dailies Aqua Comfort Plus Multifocal utilizing the same Air Optix design we all know.  But since I started fitting Clariti 1-Day Multifocal (also called Freshday Multifocal), I have to admit that I have been impressed with the results.  Like all multifocals, this lens is not perfect.  But for the design options on the market, this lens routinely is delivering the best reading vision without distance interference for a larger number of my patient base and has become my go-to daily multifocal lens.

It's the same lens, just different packaging depending on if you are a Vision Source member via

The Lens:

Clariti 1-Day is a silicone hydrogel daily lens with a Dk/t of 86 and a base curve of 8.6
Power Range = +5.00 to -6.00 in .25D steps
Add Range = LOW can accommodate up to +2.25 add, HIGH can accommodate up to +3.00
Center Near design

Fitting Guide:

Use up to date glasses Rx with vertexed distance.  Determine ocular dominance with +2.00 blur test.  The lens can tolerate up to 0.75D of astigmatism, but if the patient has greater than this don't expect clear vision.  Like all multifocal designs, performance depends on good, bright lighting for best visual performance.

There are 2 different fitting guides depending on if the patient is a hyperope or an emmetrope/ myope.  I have found that following the guide is extremely effective so definitely keep it handy!

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It is highly recommended that the initial lens from the fitting guide is dispensed on day one -- the patient will need time to adapt to the lens technology and a follow-up in about 1 week will allow that appropriate "learning" time.

At the return check up, follow these tips for trouble shooting problems:

Take Home:  There's a good reason that so many optometrists are discovering this lens is a new favorite -- it works!  It's not a miracle worker, but I have had much better patient acceptance of distance and near vision without compromise with this multifocal design than any other daily disposable multifocal to date.  It won't work for every patient, and it still requires the normal patient expectation discussions about lighting and dominance (Don't compare your eyes individually! It will look different between the eyes on purpose because that's how this lens is designed!).  For another vote of confidence, check out The Top 5 Ophthalmic Products of 2015 My Practice Can't Live Without  by Dr. Courtney Dryer.  She lists the Clariti 1-Day line of products as #1 on her list.

My advice is to keep the fitting guide with your set (or just have this post handy on your phone) and follow it exactly in initial lens selection.  I have only had to make an adjustment from this initial lens in 1 patient thus far, so it holds very true in my experience which is great for your chair time and your patient's time!

Studies suggest that up to 90% of Americans who work on a computer on a daily basis suffer from dry eye (whose symptoms include burning, redness, watering, and fluctuating vision). The culprit? One of the biggest contributing factors is that we don't blink as frequently as we normally would while at the computer.  In fact, we blink about 50% less often, when engaged in a high demand visual task (such as reading or working on your computer screen).  Since blinking mechanically releases tear film from glands in the eyelids, going longer and longer in between blinks leads to a drier and more disrupted ocular surface -- which means discomfort and blur to you!  We know that blinking is a chief issue in dry eye, but trying to get those missing blinks back has posed an even larger problem. Try telling yourself to blink every 13 seconds.  Within a few turns you'll realize you spend more time thinking about blinking than actually getting work done.  The goal of an effective solution would be to blink more without having to actively think about blinking, and the makers of Japan-based Wink Glasses are attempting to achieve just this.

Every 10 seconds the battery charged fogging of a liquid crystal sheet across the left lens of the glasses occurs for a split-second, theoretically signaling the brain to blink. via

Wink Glasses visibly signal your eye to blink by fogging for 0.1 to 0.2 seconds every 10 seconds. The momentary visual blur is intended to subconsciously trigger a blink reflex as your brain tries to "clear away" the fogged image.  Using a small battery in the left temple, fogging is achieved by inducing an electrical current through a liquid crystal sheet in the lens of the glasses.  Earlier versions of the product could be individually regulated with a sensor to track your personal blinks that would fog with a greater or less frequency if desired, but the 2013 Wink Glasses edition has simplified things to aim for that 10 second mark between fogging where most people would naturally blink if they weren't on the computer.  This streamlined version of the technology sells for around $150 in Japan, and can be upgraded with your prescription for an additional charge.  A quick search found versions available on ebay for $370 with the individualized blink setting capacity.

No reports yet of any studies being done showing an improvement in dry eye symptoms with use of Wink Glasses, but as the technology becomes more affordable and mainstream outside of Japan we should know more about its effectiveness!  Until then, if you are suffering from dry eye symptoms at your computer or workstation, remember to blink.  Try to take a break and blink every 20 minutes or so during the day to allow your eyes a chance to recover.

Love this promotional graphic from Hobson Eye Associates: "Ask use about multifocal contact lenses.. Yes, we even have dailies!"

The other day I met a woman in line at the store, pouring over magazines in the checkout.  "Look at her face -- that's not what 40 looks like! The crow's feet, the chin sag, the pores on your face getting bigger..."  It took all the reservation in my body to not say, "And don't forget about your vision!"  But maybe she hadn't admitted the awful truth quite to herself yet.  After 40, we just can't see like we used to.  The process is called presbyopia, and every day in my exam chair I try to help transition my patients in this age group in ways to enhance and ease the difficulties that come with their birthdays. We all know our population is aging --between 2000 and 2010 in the US, the population of people between the ages of 45 to 64 grew 31.5% to 81.5 million people.  But according to the 2015 Global Specialty Lens Symposium report, only 15% of all contact lens wearers are in this presbyopic age group (If you haven't read Contact Lens Spectrum's great review of the Global Specialty Lens Symposium, follow this link for more fascinating data about contact lenses in our industry). We all know people in this age group are struggling to see, but for some reason they just aren't wearing contact lenses. Why?

Obstacle 1: Comfort
The single biggest reason that contact lens wearers "dropout" of lens wear and return to glasses is due to comfort.  In fact, studies show an average of 16% of lens wearers dropout every year in the US.  In the population over 40, several other factors contribute to comfort issues beyond the contact lens material itself:

• increased computer and digital device use 
• 57% of Baby Boomers (age 51-69) have symptoms of digital eye strain and 63% of Gen Xers (age 35-50)
• increased incidence of underlying dry eye disease, especially in women
• increased incidence of demodex infestation in the eyelid (increasing ocular discomfort)
• Studies show 84% of people over age 60 have demodex mite infestation on their eyelids

British sunglass power-house Cutler and Gross has been delivering high-end fashion sunglasses for decades, but this season brings the designer's aesthetic to a duo of American based groups. For the 2015 spring/summer season they've teamed up with FRYE, an American brand known best for leather goods and cowboy boots. Their 12 piece capsule collection focuses on updates of classic American styles; familiar shapes from aviators to wayfarers get the Cutler and Gross reboot, featuring a minimalist focus on design lines and several pieces in the trending pastel color palate that was spotted all over runways this spring.

The 12 piece collection features familiar frame shapes with a gradient tinted lens. via

The Orchard Aviator via

The Mercer via

Actress Emma Roberts wearing the Mercer around the streets of New York via

I'll be the first to admit that I didn't truly understand orthoK before I attended the excellent Vision By Design conference this year.  And I don't think I was the only doctor that thought the principle of orthoK was that  you use a contact lens to forcibly press and flatten the central cornea. If this is your working model of orthoK, it's time to totally rethink everything you thought you knew!

The lens itself doesn't manually push the cornea, but the difference in dynamic forces caused by the lens design creates movement of fluid in the cornea underneath via

The biggest myth of orthoK is that the corneal mold or contact lens being used manually presses the cornea flat.  In actuality, the lens ideally won't be directly touching any part of the cornea -- there is a minimal amount of tear film underneath the lens at all times, even at the central treatment zone! Typically this area is dark when stained with NaFl dye, making doctors believe it must be an area of touch.  But levels of NaFl dye less than 20 microns thick are not visible when viewed via slit lamp, and OCT studies of on-eye relationship between lens and eye prove that there is a very slim tear film layer at all times between the eye and lens.

OCT imaging of an orthoK lens on the eye shows a thin tear film layer between cornea and lens throughout, but a larger tear fluid volume at the mid periphery. This gradient difference creates the negative pressure centrally that moves corneal fluid into the mid periphery and thus results in the desired corneal reshaping for vision treatment.  via

Corneal epithelium (top) and stroma (bottom) in an eye before orthokeratology

So how does orthoK reshape the cornea if the lens is not actually pressing on the cornea?   

After one night in orthokeratology: central corneal epithelium shows no cell loss, but there is an obvious increase is mid peripheral corneal epithelial fluid volume via

The process works because of the reverse geometry shape of the lens.  Because the central zone of the lens is much flatter than the mid periphery (return zone) of the contact lens, a negative pressure gradient is created that drives movement under the lens towards the mid peripheral areas.  What is actually moving?  Another popular misconception is that you are
pushing corneal epithelium out of the central cornea and into the mid periphery with ortho K.  In actuality, the cells aren't really changing their location, but the fluid within the cells are being redirected.  Corneal epithelial cells are connected to each other with a number of different cellular level junctions.  Gap junctions are the ones that let orthoK work -- these junctions allow fluid to pass between cells depending on osmolarity and pressure gradient. In orthoK the pressure gradient created by the orthokeratology lens shape shifts fluid between these open gap junctions towards the mid peripheral area.  As a result, the corneal epithelial cells centrally in the treatment zone are still present -- there is NO migration or loss of epithelial cells in this area!-- and the flattening effect witnessed is just the fluid movement underneath. Studies show that even after 5 years of orthoK wear, there is no loss or damage to the corneal epithelial cells.

What happens when you stop wearing orthoK lenses?  Eventually the cornea returns to its natural shape, since the corneal cells themselves have not been manipulated.  The amount of time needed to return to normal baseline varies between individuals and prescriptions.  Many doctors suggest waiting a period of 6 months without orthoK lens wear if you are wanting to have LASIK or other permanent corneal reshaping surgeries performed to ensure that the cornea is completely returned to its natural state.  What we do know is that orthoK is in no way permanent.  Any treatment effect you achieve using orthoK lenses will not last when you discontinue lens wear, and your eye is expected to return to the prescription it was before orthokeratology lenses were begun (or potentially with some slight myopic increase if they were begun on a growing child).  The largest orthoK study to date, the ongoing SMART study with an enrollment group of 200 children aged 8 to 14 has reported after 3 years of treatment an average progression of -0.17D of myopia in the treated group after 3 years of wear versus -1.01 D of progression in the control group (glasses wear) in 3 years. So while some progression of your prescription will likely still happen with orthoK lens wear, the rate of progression is greatly minimized. Stay tuned for the next post about myopia control theory -- why does orthokeratology work so well at slowing myopia progression?  We talk peripheral defocus theory in the next post of this series!

80-90% of school aged children in Asia are myopia -- creating an international epidemic of nearsightedness and a quest for a way to intervene via

If you've been paying attention to the news, you've likely heard the words "myopia epidemic." Rates of near-sightedness have been skyrocketing, with over 1/3 of the US population suffering from this visual condition (a 66% increase in the last 30 years!).  In Asian countries an estimated 80-90% of school aged children are near sighted, causing a flurry of research and attention to this growing problem.  Visual corrective aids like glasses and contact lenses can relieve blurry vision associated with this issue, but they do not prevent the eyes from getting worse year after year as a child grows.  This is the true issue with myopia -- as long as a child is growing, the eyeball can continue to lengthen every year causing higher and higher prescriptions to develop.  This pathologic progression results in high adult prescriptions, but also an increased risk of damage to the eye due to a stretched and
thinned retinal tissue, which increases the risk for potentially blinding conditions like retinal detachments, glaucoma, and macular disease processes.  For years scientists and doctors have known that myopia and its progression were the result of a combination of both genetics and environmental factors, but there was no evidence of potential treatments that could intervene in the pathologic progression of near-sightedness.  Several options now exist for parents that are eager to control the speed with which their child's prescription advances, so sooner intervention at the first signs of nearsightedness is key!