A Nutritional Approach to Contact Lens Success

Nutritional support can help mitigate dry eye, which, in turn, can improve contact lens success.


A Nutritional Approach to Contact Lens Success

Nutritional support can help mitigate dry eye, which, in turn, can improve contact lens success.

By Jeffrey R. Anshel, OD, FAAO

Contact lens fitters are all too aware of how dry eye can negatively affect successful lens wear. Contact lens wearers are five times more likely to complain about dryness symptoms compared to spectacle wearers, and more than half will report contact lens dryness, especially end-of-day dryness (Nichols et al, 2005). Discomfort is cited by more than half of patients as the principal reason for discontinuation, followed by dissatisfaction with vision (13%) (Young et al, 2002). Recent studies suggest that many contact lens wearers are not fully satisfied, and about 25% permanently discontinue lens wear (Rumpakis, 2010; Richdale et al, 2007). Patients will drop out of contact lenses unless we guard against discomfort from dryness.

This article will discuss dry eye, contact lens discomfort due to dryness, and how nutrition can play a role in mitigating dryness symptoms.

Dry Eye Definitions and Demographics

First, let’s consider the various definitions of dry eye. Dry eye syndrome (DES) is generally considered a disorder of the tear film due to either diminished tear production or excessive tear evaporation. The American Optometric Association (AOA) defines dry eye and its effects in this way: “Any condition that reduces the production, alters the composition, or impedes the distribution of the pre-ocular tear film (POTF) may cause a noticeable degradation of vision and irritation to the structures of the front surface of the eye.”

The 2007 Dry Eye WorkShop (DEWS) Report states: “Dry eye is a multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance and tear film instability, with potential damage to the ocular surface. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface.”

This condition has been referred to as “Dry Eye Syndrome” or “Dysfunctional Tear Syndrome,” among others. Considering the inflammatory component, many believe that it should now be called “Dry Eye Disease.”

Dry eye affects more than 5 million older Americans, and it is particularly prevalent among women (Schaumberg et al, 2003). Tens of millions more may have a less severe manifestation of the disease. This condition is increasing every year and is prevalent in 75% of Americans over age 65 (Richdale et al, 2007).

The Tear Film and Ocular Surface Society (TFOS) recently completed a workshop on contact lens discomfort (CLD) (Nichols et al, 2013). The workshop defined the current state of CLD as “a condition characterized by episodic or persistent adverse ocular sensations that can ultimately lead to decreased wearing time or discontinuation of contact lens wear.” The defined categories were divided between discomfort due to the contact lens or due to the environment, and each of these categories is subsequently broken down into four additional factors. The category that we will consider here is modifiable patient factors, specifically nutrition.

Role of the Tear Film

The theory of the dry eye disease process is that the tear film destabilizes, initiating desiccation of the ocular surface. This allows injurious agents (free radicals, toxins, microbes, etc.) to cause an inflammatory reaction that allows cytokines to affect the ocular surfaces, epithelium, and lacrimal glands (Kyminosis et al, 2008).

The tear film is a complex structure composed of water, salts, enzymes, proteins, immunoglobulins, lipids, metabolites, and exfoliated epithelial and polymorphonuclear cells (Rolando and Zierhut, 2001). When contact lenses dehydrate, the internal hydrophobic regions of tear proteins—including albumin, lactoferrin, and lysozyme—bind to the hydrophobic regions of the material.

To improve patient comfort, we need to understand how contact lenses affect the tear film. Tear film thickness is important as it determines the tear volume from which evaporation occurs. The tear film is very thin; it measures about 7 microns by invasive estimates and 3 microns by newer, non-invasive techniques (King-Smith et al, 2000). It consists of the outer lipid layer, which comes primarily from the meibomian glands along the lid margin; the middle aqueous layer, mainly from the lacrimal gland in the upper eyelid; and the mucin layer from the conjunctival goblet cells and superficial corneal epithelial cells.

Mucins are highly hydrophilic and fill in the gaps of the epithelial microvilli to provide a smooth optical surface and to make the eye more wettable. Electrolytes in the aqueous layer are responsible for tear osmolarity and pH maintenance. Proteins in the aqueous layer are markers of biological function. The lipid layer is the major barrier to evaporation, and is actually the first refracting surface for light entering the eye. New studies suggest that the tear film is more dynamic than this traditional three-layer model, with mixing occurring between the mucin and aqueous layers to form a complex hydrated gel (Peters and Colby, 2006).

Blinking spreads the tear film across the ocular surface, eventually thinning through evaporation, which stimulates the next blink. Tears from the tear prism move by capillary action to the puncta and exit through the ducts. As well as providing comfort to the anterior eye, the tear film has an important role in maintaining vision, preventing desiccation, supplying essential nutrients to the cornea, removing debris, and helping prevent infection (DEWS Report, 2007).

Diagnosing Dry Eye

Dry eye is now recognized as a disturbance to the lacrimal functional unit (LFU) (Stern et al, 2004). The LFU, comprising the lacrimal glands, ocular surface, lids, and the nerves that connect them, controls tear film stability and is regulated in response to the environment and intrinsic influences. Damage to any part can destabilize the tear film, leading to ocular surface damage, dry eye symptoms, and changes in vision. Aqueous deficient dry eye and evaporative dry eye have been removed from the dry eye definition, but are still helpful to explain pathogenesis.

Tear Osmolarity Tear film hyperosmolarity is often suggested to be the one underlying factor that is common to all forms of dry eye, resulting in corneal epithelial cell apoptosis and stimulation of inflammatory cells (Gilbard, 1994). Osmolarity is now part of the definition of dry eye and may be the “signature” feature of ocular surface dryness, although osmolarity values do not differentiate between the sub-types (Gilbard, 1994).

One instrument developed to measure osmolarity clinically is the TearLab Osmolarity system (TearLab Corp.); it may also help to monitor the effectiveness of treatments. Now that the TearLab Osmolarity System is commercially available, we can utilize tear osmolarity as a key dry eye diagnostic tool. The TearLab osmometer can measure osmolarity on a 50nL sample and record an average within run coefficient of variation of 1.47%, which corresponds to a precision of ±4.5 at 308.7mOsm/L (Gilbard, 1994). Nichols et al (2006) found that the tear film osmolality was significantly higher in contact lens patients who have dry eye when compared to contact lens patients who don’t have dry eye.

Diagnosing Contact Lens Discomfort

CLD related to dryness is a marginal, rather than overt, disease state. Patients are often asymptomatic prior to initiating contact lens wear and can develop dry eye symptoms without obvious signs. The DEWS Report (2007) also recognizes asymptomatic patients who will exhibit dry eye signs without complaint. It is likely that these patients have accepted symptoms as a matter of course. The essential message is that symptoms don’t always match signs, and “happy” contact lens wearers should still be investigated.

Although the exact pathogenesis of CLD is unknown, most agree that one of the major factors for successful contact lens wear is a stable tear film. The tear film lubricates and hydrates the contact lens; therefore, it is essential to contact lens comfort. Because CLD is complex and likely multifactorial, there are many potential mechanisms.

New techniques help us understand how contact lenses affect tear film stability. A contact lens splits the tear film, creating a pre-lens lipid-aqueous layer and a post-lens aqueous-mucous layer. Deposition of proteins, lipids, and mucins occurs relatively quickly after lens application. Deposits may come from the tears (Figures 1 and 2), the environment, or even from handling of the contact lenses.

Figure 1. Lipid on silicone hydrogel lens after two weeks of wear.

Figure 2. Tear film smear on a fresh silicone hydrogel lens 20 minutes after application caused by too rapid pre-lens tear film breakup.

CLD most likely begins with pre-tear film disruption, when eyelid conditions begin to compromise the dynamics and chemistry of the tear film. Contact lens wear thins the tear film and increases the tear film thinning rate through a complex process of evaporation and dewetting. This evaporative dry eye type is mainly caused by meibomian gland dysfunction.

Pre-lens thinning time is 2.8 seconds faster in patients who have dry eye symptoms compared to those who do not (Nichols and Sinnott, 2006). The thinning is thought to occur in the lipid layer, which forms discrete islands on the front surface of the contact lens. An average tear volume is 0.728mm3, while the volume of a lens is 34.693mm3. So, with a lens in place, the tear film now has to cover double the original surface area. Interference with the lipid layer results in up to a 50% increase in evaporation and rapid drying of the tear film and the contact lens, which also may attract lipid deposits from the tear film, with the result that the lens fails to wet (Nichols and Sinnott, 2006). Vision also can be affected if the tear film fails to fill in the irregularities of the corneal epithelium, and optical deterioration has been measured objectively in contact lens wearers post-tear film breakup (Nichols and Sinnott, 2006).

In a study of 360 hydrogel GP contact lens wearers, Nichols and Sinnott (2006) found that CLD may be explained by increased pre-lens tear film thinning times and increased tear film osmolality. An increase in pre-lens tear film thinning time can be attributed to evaporation of the tear film itself secondary to an altered lipid layer, and to lens dewetting secondary to hydrophobic regions on the lens surface.

An aqueous deficient type can potentially result from reduced lacrimal stimulation due to reduced corneal sensitivity that occurs with prolonged contact lens use. Osmolarity increases in both subtypes, causing damage to the surface epithelium and discomfort, and it can lead to a chronic inflammatory condition such as keratitis.

Predicting Dry Eye in Contact Lens Wearers

Predicting which contact lens patients are more likely to develop dry eye can help you set realistic patient goals and tailor management to individual patients. Conjunctival parallel folds and lid wiper epitheliopathy appear to be predictive for dry eye (Korb et al, 2002). Lid wiper epitheliopathy is damage on the upper eyelid edge (which will stain with lissamine green) from repeated blinking over a poor tear film. Lid parallel conjunctival folds, another possible consequence of lid friction, are small folds in the lower quadrant of the bulbar conjunctiva, parallel to the lower lid margin (Höh et al, 1995).

Technology advances are now ubiquitous in today’s society. We look at digital screens for a significant part of our workday, and our eyes are being taxed to their limit. Staring at such screens reduces the blink rate, resulting in more tear film evaporation and exposure of the ocular surface. Given this, it is no wonder that dry eyes are a common complaint among computer users. Caution these patients about incomplete blinking, prolonged computer use, and the problems of low humidity, drafts, and drying systemic drugs (e.g., antihistamines, decongestants, beta-blockers, hormone replacement therapy, antidepressants, and some psychotropics) (Korb et al, 2002). Positioning the computer monitor below eye level decreases the interpalpebral aperture exposure (Bentivoglio et al, 1997).

Supplements and Nutrition

Prior to 2011, there were few studies on the mechanism of using essential fatty acids (EFAs) as a treatment for dry eyes. Since then, there have been only four randomized clinical trials on omega-3 EFAs, and the results are promising. However, we’ve been recommending them for our patients for many years prior to that time without significant scientific support for the practice.

Oral nutritional formulations of EFAs are being used to treat DES, some with more success compared to others. For EFAs to be an effective treatment for DES, there must be a proper balance of both omega-6 and omega-3 EFAs from chemically stable plant oil to consistently produce series 1, tear-specific, anti-inflammatory prostaglandin (PGE1). EFA treatment of DES is dependent on specific nutrient co-factors that aid the downstream metabolic conversion to anti-inflammatory prostaglandins. These nutrient co-factors also stimulate the production of healthy goblet cells as well as enhance production of clearer and thinner meibomian gland oil production (Sullivan et al, 2000). EFA formulations will also block arachidonic acid (AA) fatty acid cleavage to the series 2 cyclooxygenase enzyme (COX-2), which can convert to a pro-inflammatory, series 2 prostaglandin (PGE2) without the nutrient co-factors that inhibit the formation of COX-2 (Dommels et al, 2003) (Figure 3).

Figure 3. Metabolic pathway of essential fatty acids.

Properly designed formulations will also stimulate lacrimal gland secretion as well as the production of tear lactoferrin, which is the anti-viral, anti-bacterial, iron-binding protein that is particularly vital to post-LASIK and other postoperative patients (Pisella et al, 2002).

The nutritional formulations that are designed around chemically stable omega-6 plant oils all contain linoleic acid (LA) and significant amounts of gamma linolenic acid (GLA), plus the nutrient co-factors necessary to ensure the delta-6-desaturase (D6D) enzymatic metabolic conversion to the tear-specific, anti-inflammatory PGE1 (Barabino et al, 2003; Kokke et al, 2008). They also contain varying amounts of omega-3 alpha-linolenic acid (ALA), which converts to docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). To back up this plant-based ALA/DHA/EPA conversion, formulations should include small amounts of mercury-free fish oil, which contains DHA and EPA, necessary to block the delta-5-desaturase (D5D) enzymatic AA cleavage of the omega-6 downstream dihomo-gamma-linolenic acid (DGLA) metabolite by the COX-2 enzyme (Barham et al, 2000). This enzyme, if not blocked, can convert omega-6 DGLA to the pro-inflammatory PGE2. Early dry eye nutritional products did not address the AA/COX-2 cleavage issues as they pertain to the downstream conversion of EFAs to anti-inflammatory prostaglandins.

Some manufacturers are designing formulations that are focused on the metabolic action of the omega-3 EFA, which is primarily found in flax and fish oils. The omega-3 EFA also requires nutrient co-factors to consistently convert downstream to DHA and EPA, which subsequently convert to the anti-inflammatory PGE3. PGE3 is an important site-specific anti-inflammatory, particularly for rheumatoid arthritis patients, but is not as specific to tears compared to the PGE1 from the omega-6 fatty acid metabolites (Johnson et al, 1997). The anti-inflammatory PGE1s from natural omega-6s are more specific to mucosal tissues (eyes) than are the PGE3s from omega-3s (Barabino et al, 2003).

Researchers from Louisiana State University, New Orleans, reported that resolvins from EPA increase tear volume and decrease inflammation induced by dry eye, while topical application of DHA following corneal surgery was also shown in an animal trial to increase corneal epithelial cell proliferation (Li et al, 2010). The researchers also found that resolvin E1 encourages tear production, corneal epithelial integrity, and a decrease in inflammatory inducible COX-2. Most recently, they noted that while no firm recommendation for human use of DHA/EPA in DES can be made based only on the animal trials, the EFAs could prove useful in humans due to their apparent ability to resolve inflammation and to regenerate damaged corneal nerves.

Some practitioners still recommend flax oil as a stand-alone treatment for DES, as it contains a large amount of omega-3 and a small amount of omega-6. Unfortunately, flax oil is highly unstable and contains none of the nutrient co-factors necessary to ensure the consistent enzymatic conversion to either PGE1 or PGE3; nor does it enhance the production of tear lactoferrin (Wu et al, 1999). The same can be said for any of the plant-based omega-3 fatty acids. While they may have some anti-inflammatory effect in women (conversion rate of about 10%), it’s unlikely that men would benefit from flaxseed oil, due to a poor conversion rate of about 1% (Lane et al, 2011).

Do not confuse processed food items that contain hydrogenated trans-fats with omega-6 essential fatty acid intake. All fatty acids are destroyed by the hydrogenation process. Food sources for EPA and DHA are typically small, fatty fish such as mackerel, tuna, salmon, sardines, and anchovies. All supplement pills made from these fish are FDA inspected for purity and certified free from polychlorinated biphenyls (PCBs) and mercury. The argument regarding the pros and cons of ethyl ester versus triglyceride forms of fish oil is beyond the scope of this article, but worth considering when looking for a suitable supplement for your patients. A food source with the best balance of omega-6 (GLA) and omega-3 is black currant seed oil (typically a 4:1 ratio).

Additional nutritional support also can be provided for the tear film. Magnesium and zinc support immune function. Aloe vera and hyaluronic acid enhance the mucins. Vitamins A and D support epithelial cells and immune function (McCullough et al, 1999). Vitamin B6 supports neuronal blink response and GLA-to-DGLA conversion (Zhao et al, 2012). Vitamin C enhances the production of IgE concentrates in tears (Wolvers et al, 2006). Vitamin E slows lipid oxidation (Fujikawa et al, 2003). Lactoferrin can also be used (Fujikawa et al, 2003). Serum lactoferrin is released from the eyelid in a manner similar to serum IgG, and possibly from tear neutrophils during infection and inflammation; by binding iron, it prevents the pathogen from obtaining sufficient iron for growth.

Nutritional supplements can play an important role in managing inflammation associated with dry eye by enhancing the body’s natural defense system, and the protection provided by nutritional therapy may be better than after-the-fact treatment by pharmaceuticals.


A multi-pronged approach is recommended to achieve successful contact lens wear. We should strive to minimize adverse environmental conditions, consider anticholinergic medications, and reduce visual strain. Nonpreserved artificial tears can still serve as an adjunct therapy if patients experience discomfort due to dryness symptoms, but topical corticosteroids should be used only for brief periods of time because of side effects. You might consider topical cyclosporine for severe cases.

Consider performing a nutritional panel blood workup with laboratory tests that will quantify the serum nutritional levels. But overall, the treatment should not cause disruption in patients’ lifestyles. Most patients prefer a “natural” approach first. CLS

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Dr. Anshel is the principal of Corporate Vision Consulting, where he addresses the issues surrounding visual demands while working with computers. He also maintains a private practice in Carlsbad, Calif., and is the founder and president of the Ocular Nutrition Society. He has written numerous articles and five books regarding nutritional influences on vision and computer vision concerns. He lectures nationally to eyecare practitioners on nutrition topics.