Eye of an older man developing cataracts



Last Section Update: 10/2020

Contributor(s): Shayna Sandhaus, PhD

1 Overview

Summary and Quick Facts for Cataracts

  • Cataracts are the most common cause of blindness and are generally treated with surgery. The formation of cataracts is associated with diabetes, but many people may not be aware that higher-than-normal blood glucose levels, even if not clinically considered diabetes, can contribute to cataracts.
  • In this protocol you will not only learn how cataracts form and what causes them, but also how dietary and lifestyle considerations may help prevent cataracts and slow the progression of lens opacification. Conventional treatment of cataracts will be discussed, as will some novel and emerging therapeutic strategies that may improve treatment outcomes.
  • By proactively managing identified risk factors for cataracts, one may be able to reduce their onset and/or progression. Natural interventions including antioxidants such as vitamin C and riboflavin, as well as glycation inhibitors such as carnosine and carnitine, may help reduce the risk of cataract formation.

What are Cataracts?

Cataracts are opacities that form in the lens of the eye, causing visual obstruction. They arise when proteins in the eye form aggregates due to incorrect three-dimensional structure. There are several factors that cause proteins to aggregate, including oxidative stress and glycation. Cataracts are the most common cause of blindness and are generally treated with surgery.

The formation of cataracts is associated with diabetes, but many people may not be aware that higher-than-normal blood glucose levels, even if not clinically considered diabetes, can contribute to cataracts.

Natural interventions including antioxidants such as vitamin C and riboflavin, as well as glycation inhibitors such as carnosine and carnitine, may help reduce the risk of cataract formation.

What are the Risk Factors for Cataracts?

  • Age
  • Gender – women are more likely to develop cataracts
  • Poor nutrition
  • Diabetes
  • Exposure to ionizing radiation such as X-rays or UV rays
  • Smoking and drinking alcohol
  • Genetic predisposition

What are the Signs and Symptoms of Cataracts?

Note: Depending on the type of cataract, the symptoms can vary. Some common symptoms of the different types of cataracts include:

  • Seeing double or multiple images
  • Difficulty distinguishing colors
  • Glare or halos around lights
  • Impaired ability to see in bright lights

How are Cataracts Conventionally Treated?

  • Surgery

What Emerging Therapies Appear Promising for Cataracts?

  • Combining non-steroidal anti-inflammatory drugs (NSAIDs) with surgery
  • Statins

What Dietary or Lifestyle Changes Can Help Prevent Cataracts?

  • Quitting smoking
  • Limiting exposure to UV radiation by wearing sunglasses
  • Limiting alcohol consumption
  • Increasing intake of fruits and vegetables, as they are natural sources of antioxidants
  • Avoiding foods high in saturated fats and consuming more omega-3 fatty acids
  • Controlling blood glucose levels

What Natural Interventions May Be Beneficial for Preventing Cataracts?

  • Glutathione. Glutathione scavenges free radicals in the lens, preventing oxidative damage to the proteins.
  • Vitamin C. Vitamin C acts as an antioxidant to support healthy proteins in the lens and is linked with lower incidence of cataract development.
  • Vitamin B2 (riboflavin). Riboflavin is an essential component of flavin adenine dinucleotide (FAD), which is used by the enzyme that converts glutathione to its bioactive form. High riboflavin levels have been associated with reduced risk of cataract formation.
  • Vitamin B6. Vitamin B6 has been shown to reduce the production of advanced glycation end products (AGEs) in diabetic lenses.
  • Vitamin E. Vitamin E acts as an antioxidant and low levels are associated with an increased risk of developing cataracts.
  • Other antioxidants and glycation inhibitors that can help prevent cataracts are N-acetylcysteine,lipoic acid, melatonin,carnosine, carnitine, and quercetin.
  • Carotenoids. Carotenoids (a type of plant pigment) such as lutein, zeaxanthin, and meso-zeaxanthin can absorb light and prevent damage caused by UV rays. They are found in high concentrations in the eye and can help prevent cataract formation.
  • Other interventions for healthy eyes include bilberry, green and black tea, resveratrol, and selenium.

2 Introduction

As we age, the lens of the eye can become clouded, impairing vision. These opacities in the normally transparent lens are called cataracts, and represent the most common cause of blindness (MedlinePlus 2012). Almost 25 million people worldwide have vision loss as a result of cataracts, which accounts for over 47% of blindness globally (Resnikoff 2004; West 2010; Allen 2011; Hashim 2012). More than 50% of people in the United States over age 80 either have cataracts or have undergone surgery due to this condition (MedlinePlus 2012).

While cataracts are a significant impairment, they can be surgically treated by removing the original lens and replacing it with a long-lasting synthetic lens. Though there are no FDA-approved drug treatment options for cataracts (Yanoff 2013), cataract surgery represents one of the most successful interventions in medicine (Lichtinger 2012).

Although conventional surgical treatment is an important consideration in the management of advanced cataracts, the medical establishment often fails to emphasize the need to maintain healthy blood glucose levels to slow progression or prevent onset of cataracts. Most physicians appreciate the association between overt diabetes and cataracts, but many overlook the role of elevated blood sugar in cataract formation among non-diabetics (Aoki 2007; Drexler 2001; Jessani 2009). The lens of the eye is particularly susceptible to glycation reactions, in which high glucose concentrations damage proteins and contribute to tissue dysfunction (Jain 2002; Pereira 1996; Franke 2003). A number of human studies have associated higher-than-normal glucose levels with substantially increased risk of various types of cataract (Weintraub 2002; Kanthan 2011; Saxena 2004; Tan 2008). Sadly, although it may be possible to prevent cataracts or slow their progression simply by controlling blood sugar levels (Taylor 1995; Madar 1993, 1994; Cohen-Melamed 1995), many at-risk individuals remain unaware of the profound impact of elevated glucose levels on the lens of the eye.

In this protocol you will not only learn how cataracts form and what causes them, but also how dietary and lifestyle considerations may help prevent cataracts and slow the progression of lens opacification. Conventional treatment of cataracts will be discussed, as will some novel and emerging therapeutic strategies that may improve treatment outcomes. The role of targeted natural interventions in combating specific disease processes that underlie cataract development, such as oxidative stress and glycation, will be examined as well.

3 Understanding the Eye and the Lens

The eye, arguably the most important sensory organ, has evolved to provide detailed imagery of the world around us in much the same way that a camera provides a photographer with a picture. Like a camera, the eye contains a series of internal structures instrumental to its function. Like a camera’s lens shutter, the cornea represents a protective layer of cells that help refract light. As with a camera’s lens, the main function of the optic lens is to refract light and help focus it on the retina, where images are processed into signals that can be interpreted by the brain via the optic nerve. The proper function of the lens hinges on its transparency (MedlinePlus 2012).

The lens can be thought of as a light-permeable barrier consisting of two major components: an epithelium and a mass of fiber cells. The epithelium, which is a single layer of cells nearest the front of the eye, provides protection to the interior layers. The inner mass of elongated fiber cells ensures the transparency of the lens (Bhat 2001). Maintenance of healthy structure and function of the lens depends on proper functioning of complex cellular machinery, which if compromised, can lead to decreased lens transparency (Mathias 2010; Michael 2011).

4 Causes and Risk Factors

Oxidative Stress

Living cells are naturally exposed to free radicals including reactive oxygen species (ROS) (Michael 2011; Colorado State University 2013). Mitochondria (cellular organelles) produce free radicals as a by-product of their normal function (Cadenas 2004). These free radicals can damage other cellular structures such as proteins, lipids, and DNA. Exposure of cells to excess oxidative stress that overwhelms intrinsic antioxidant defenses can lead to cellular dysfunction and destruction (Carper 1999; Uttara 2009). The lens epithelium is particularly sensitive to oxidative stress, and oxidative damage of this layer of cells can result in the formation of lens opacities (Carper 1999; Sharma 2009).

Many diseases are associated with the incorrect folding of proteins as a result of oxidative damage. The three-dimensional structure of proteins dictates their function; therefore, any structural damage to proteins can lead to their malfunction. Since the protein concentration in the lens is the highest in the body, the lens is vulnerable to this type of perturbation (Surguchev 2010).

The transparency of the lens depends on the correct three-dimensional structure of the lens proteins, and protein aggregation in the lens has been linked to the formation of cataracts (Moreau 2012). This is especially true when antioxidant mechanisms fail to prevent oxidative damage, causing a cascade of damage to several types of proteins in the lens (Carper 1999; Babizhayev 2010). One type of lens protein known to cause cataracts when damaged is the crystallins (Sharma 2009). Crystallins provide structural support to lens cells and allow for the optimal bending of light as it enters the lens (Bloemendal 2004; Sharma 2009). 


In addition to oxidative stress, studies have uncovered a causative role for another modification, known as glycation, in the opacification of the lens (Swamy 1987). Glycation causes proteins to become damaged and dysfunctional. It is the result of sugar molecules interacting with proteins and modifying their structure. Proteins in the lens, which are among the longest-lived in the body, are particularly susceptible to glycation (Franke 2003).

The result of this interaction is the formation of toxic molecules termed advanced glycation end products, or AGEs. Accumulation of AGEs is associated with several age-related diseases including diabetes, renal failure, and cataracts (Wautier 2001; Hashim 2011; Swamy 1987; Wautier 2001; Franke 2003; Gul 2009). Additionally, AGE accumulation is thought to be directly related to the intensity of yellowing of the lens, which is often observed in cataracts (Shamsi 2000).

Risk Factors

In addition to the pathological roles of oxidative stress and glycation in cataract formation, several factors are known to increase cataract risk. Many of the following risk factors are associated with increased glycation and/or oxidative stress.

Age. There is a strong association of cataract development with age and oxidative damage. Since there is no turnover of lens epithelial cells, the accumulation of oxidative damage over many years is an important component of cataract development (Truscott 2005).

Gender. Although cataracts afflict both men and women, a study in an Australian population revealed that 58% of people who have suffered from cataracts are women, and a higher incidence of cataracts in women is supported by studies on other continents (Giuffrè 1995; Delcourt 2000; Kanthan 2008; Mares 2010; Vashist 2011). 

Poor Nutrition. Lack of a proper diet and low intake of vitamins, minerals, and antioxidants found in fruits and vegetables predispose people to developing cataracts (Jacques 1988; Bunce 1990; Knekt 1992; Christen 2005; Zhou 2012).

Diabetes. There is a strong association between duration of diabetes and the development of cataracts (Kim 2006; West 2010). In people with diabetes, cataracts may begin to form up to 20 years earlier than in non-diabetics (Hashim 2012). Since diabetes is characterized by elevated blood sugar, glycation reactions occur more rapidly and frequently in this population, which explains a great deal of the association between diabetes and cataracts (Hashim 2011).

Exposure to Ionizing Radiation. Occupational or personal exposure to ionizing radiation, such as X-rays or ultraviolet (UV) rays, is associated with an increased risk of developing cataracts (Worgul 1976; Vano 2010; Varma 2011). In order to decrease exposure of the lens to UV radiation, it is recommended that protective eyewear or sunglasses with UV filters be worn during daylight hours.

Smoking Status and Alcohol Consumption. There is a significantly increased risk for cataracts for those who smoke and among those who drink alcohol heavily (Delcourt 2000; Klein 2003; Jun 2009).

Genetics. When cataracts form in newborns, they are often associated with mutations in proteins involved in metabolic pathways related to the metabolism of a sugar called galactose, while mutations in structural proteins like crystallins occur frequently in childhood cataracts (Churchill 2011; Santana 2011; Chan 2012; Clark 2012).

Additional factors have been implicated in the development of some types of cataracts, but more studies need to be conducted to determine the strength of these relationships (Heiba 1995; Merriam 1996; Sanderson 2000; Zhou 2007; Jun 2009; Hashim 2012; Worgul 1976; Alapure 2012; Paine 2010; Tsai 2003; Vano 2010):

  • Imbalanced calcium ion signaling
  • Long-term steroid (glucocorticoid) use

5 Signs and Symptoms

There are three main types of age-related cataract, determined by which part of the eye they affect; they each can cause different symptoms:

  • Nuclear cataracts. Nuclear cataracts affect the central part of the lens. Nuclear cataracts arise as a result of normal age-related accumulation of lens fibers in the central region of the lens. Patients with nuclear cataracts may see double or multiple images. As the cataract progresses, the lens transitions to yellow or brown, and this may lead to even more difficulties in distinguishing colors (Medline 2012; Bollinger 2008).
  • Cortical cataracts. Cortical cataracts are the result of the formation of whitish opaque regions at the outer edge of the lens, or the cortex. This type of cataract is associated with diabetes (Chang 2011). Cortical cataracts may not significantly impair vision if the lens opacities remain outside the visual axis, but they can cause glare during activities such as driving (Medline 2012; Bollinger 2008).
  • Posterior subcapsular cataracts. Posterior subcapsular cataracts first appear on the backside of the lens. They typically impair near vision to a greater degree than distance vision. In addition, they may affect the ability to see in bright light and cause the appearance of halos around lights during nighttime (Medline 2012; Bollinger 2008).

In addition to age-related cataracts that appear in adults, some children are either born with cataracts or develop them early in childhood. About half of congenital cataracts have genetic causes, while some of the remaining ones are caused by metabolic diseases or infections during development (Santana 2011; Medline 2012). 

Early Stages of Cataract Development

Age-related cataracts cause a slow, painless loss of vision typically not associated with other signs or symptoms. The first sign of cataracts is usually a significant loss in transparency in a small region of the lens. This affects one’s ability to discern the detailed contours of objects in bright light during the day or when viewing objects near bright light at night. In addition, it leads to a loss of contrast sensitivity, which is the ability to distinguish between relative differences in light intensity (Regan 1993; Cheng 2001; Zigler 2011; Sia 2012).

Similar to a loss in contrast sensitivity is the increased incidence of glare. This occurs when cataracts begin to cause an aura around objects, and it happens most often during the daytime (Lasa 1995; Howes 2008; Mayo Clinic 2010).  Glare, which can occur in all forms of cataract, can develop anywhere on the optic lens.

In many cases of nuclear cataract formation, there is also a change in how light bends, or refracts, as it moves from outside the eye through the lens. This is termed myopic shift, and is clinically defined as a hardening of the lens that causes a change from farsightedness to nearsightedness (Younan 2002; Aslam 2007; Samarawickrama 2007; Zigler 2011).

Late Stages of Cataracts

As cataracts continue to progress, the severity of these initial symptoms increases. The extent of cataract progression is defined by the degree of opacity in that part of the lens and the overall state of visual acuity.  Immature cataracts are determined as those occurring in lenses with significant areas of translucency. Progression to mature cataracts is marked by significant opaque structures occurring in the lens, while hypermature cataracts are those where liquefaction of the lens structure has occurred. This final stage of cataract development results in the leakage of a milky white liquid into the lens capsule, resulting in substantial inflammation and pain (Hemalatha 2012).

6 Diagnosis and Conventional Treatment

Cataracts are diagnosed by an ophthalmologist using the Snellen visual acuity test. In this test, the patient is asked to read letters that become smaller on every line, and the ability to recognize them is measured (Levy 2005; Medline 2012). Once suspected, cataracts are assessed using a specialized microscope that focuses light into a slit to examine the lens structure. It measures not only the visual acuity, but also the degree of light scattering, which is the transmission of the light in random directions when the environment that it crosses presents irregularities (van der Mooren 2011; Medline 2012). Cataracts are also detected using a device known as a funduscope or ophthalmoscope, which is used to examine the retinal blood vessels and other structures of the eye by inspection (Schneiderman 1990; Merck 2012). The inability to see the retinal blood vessels usually occurs because of an opacity that interferes with the ability of the light to pass through the eye, and this is usually caused by cataracts or bleeding inside the eye (Schneiderman 1990).

Once diagnosed, and after the stage and severity of the cataracts are assessed, a patient may elect to undergo surgical removal of the lens containing the cataract(s) and replacement with a synthetic intraocular lens (IOL). In these procedures, which usually last for less than an hour and are normally performed on an outpatient basis, surgeons make a small incision on the lens, disrupt the lens either ultrasonically or by using lasers, and insert the IOL into the capsule bag where the natural lens used to be located (Medline 2012).

If a cataract is so advanced that this procedure is unable to break up the lens, then a larger incision is made, and the lens nucleus is removed through the exposed lens capsule. The soft portions of the lens near the edges are removed using a vacuum, leaving a shell for IOL implantation. Referred to as extracapsular extraction, this surgical process can result in higher rates of secondary infection and other complications (eg, secondary cataracts) (Smith 1982; Ruit 1991; Apple 1992; Gyldenkerne 1998; Clark 2000; Haripriya 2012; Medline 2012; Merck 2012).

Other complications that may occur include swelling of the cornea, retinal detachment, internal eye infections, secondary glaucoma, excessive post-operative inflammation, capsular opacification, and other conditions that may result in permanent partial or complete loss of eyesight (Morikubo 2004; Franzco 2010; Speeg-Schatz 2011; Haug 2012; Taravati 2012).

Even without suffering from a serious complication, a significant number of people who have cataract surgery go on to develop clouding of the lens capsule (Pandey 2004; Eichenbaum 2012; Lichtinger 2012). This complication may occur at various times after surgery, usually three months to four years later (Pandey 2004). In these cases, the lens capsule, which was originally part of the lens previously removed, will require additional laser surgery. This complication has medical and financial implications, including additional medical care costs, time off from work, and patient suffering (Pandey 2004; Eichenbaum 2012). Younger patients are at higher risk for this complication (Pandey 2004).

If surgical removal of a lens with a cataract is inadvisable, or if significant loss of visual acuity has not occurred, ophthalmologists may suggest delaying surgery (National Eye Institute 2009; Medline 2012). Cataract surgery may also be inadvisable if the patient suffers from other forms of ocular disease, such as age-related macular degeneration, which was reported by some clinicians to worsen after cataract surgery (Casparis 2012). In the interim, patients are advised to use soft contact lenses or eyeglasses with stronger prescriptions and to adopt alternative treatment strategies (National Eye Institute 2009).

Secondary Cataracts

Secondary cataracts arise when, after surgery, lens epithelial cells divide and move to the back side of the lens where they transform into another cell type; the light-scattering changes they cause result in the secondary loss of vision (Coombes 1999; Marcantonio 1999; Wormstone 2009). This complication can also be thought of as a wound healing response that occurs after surgery (Bertelmann 2001). The rates of secondary cataract formation vary; some sources indicate that they may occur in up to 50% of patients, and while advances in surgical techniques helped lower their frequency in recent years, they were still reported to occur in 14-18% of patients, and remain a major complication (Coombes 1999; Spalton 1999; West-Mays 2010). They occur even more frequently and have a quicker onset in children (Awashti 2009). Secondary cataracts are easy to treat using laser treatment, and the risk of complications is small (Emery 1998; Spalton 1999). Immunological and gene therapy approaches to prevent this complication are under development and appear promising (Bertelmann 2001; Saika 2008).

7 Novel and Emerging Medical Therapies and/or Drug Strategies

Combining NSAIDs with Surgical Removal of the Affected Lens

One active area of anti-cataract research is that of non-steroidal anti-inflammatory drugs (NSAIDs). These drugs work by inhibiting enzymes that promote inflammation (Kim 2010). NSAIDs have been evaluated in several clinical trials, and there is evidence that when applied locally, they can reduce inflammation after cataract surgery (Kim 2010). NSAIDs appear from some studies to be more effective than corticosteroids in certain respects, and other studies reported that the two have additive effects (Kim 2010). When administered after the surgical removal of the lens, NSAIDs have been shown to help reduce post-surgical complications (eg, excessive fluid build-up, pain, and swelling) by reducing inflammation (Wittpenn 2008; McColgin 1999). Research is ongoing to compare NSAIDs and determine which are the most effective after cataract surgery (Cho 2009; Bucci 2011; Bradley 2013).

Statin Drugs

Some early observational studies suggested an association between long-term statin use and an increased chance of developing cataracts, while others found marginal or no risks (Derby 2000; Jick 2001; Machan 2012). However, clinical research showed that statins may actually lower the risk of developing cataracts, with a 50% decrease in the risk of mainly nuclear and cortical cataracts in one study (Klein 2006; Tan 2007). Another study demonstrated that the potential beneficial effects of statins are present with longer duration of statin administration, finding protective effects against cataract surgery in patients aged 50-64 (Fong 2012). Although these discoveries may provide a new therapeutic application for statins, additional research is required to understand what formulations of statins are required to prevent cataract formation as well as how statins may prevent cataracts.

8 Dietary and Lifestyle Management Strategies

By proactively managing identified risk factors for cataracts, one may be able to reduce their onset and/or progression. The following lifestyle management strategies center on avoiding oxidative damage and glycation reactions in the lens (National Eye Institute 2009):

  • Quitting smoking, since toxins from tobacco smoke damage proteins such as crystallins (Randerath 1992; Paik 2000)
  • Limiting or eliminating exposure to UV radiation from the sun
  • Avoiding work-related exposure to X-rays and gamma irradiation
  • Limiting or reducing the consumption of alcohol

In addition to these lifestyle changes, numerous studies revealed that food-based antioxidants are useful in the treatment of cataracts (Agte 2010). By increasing the consumption of foods rich in antioxidants and phytochemicals, such as vegetables and fruits, the human body may be able to more effectively scavenge and eliminate free radicals and reactive oxygen species. 

Other dietary considerations include avoiding meats high in cholesterol and saturated fats (eg, fatty cuts of beef, processed meats) and consuming more fish rich in omega-3-fatty acids (eg, salmon). Nuts and seeds, particularly walnuts and flaxseed oil, are additional sources of omega-3 fatty acids (Psota 2006). Omega-3 fatty acids were shown to protect against oxidative damage caused by UV radiation in other tissues, and since the development of cataracts was causally linked to oxidative damage in the lens, this action could represent another mechanism by which they protect against cataract formation or progression (Rhodes 2003; van der Pols 2011).

Controlling Blood Glucose Levels to Prevent Cataracts – Even in Non-Diabetics

Diabetes is a well-known risk factor for cataracts (Rowe 2000; Heydari 2012), but the link between elevated blood glucose levels and cataracts is less appreciated in non-diabetics.

Even in people without overt diabetes, elevated blood sugar causes significant damage throughout the body by increasing oxidative stress and promoting protein-destroying glycation reactions, leading to a number of chronic diseases (Paik 2012; McNeilly 2011; Nitenberg 2006; Miyazawa 2012; Lindsey 2009). The lens of the eye is particularly susceptible to damage associated with elevated glucose (Jain 2002; Pereira 1996; Franke 2003).

Researchers at Harvard University conducted a meticulous analysis on more than 87 000 individuals over a 16-year period and concluded that “[posterior subcapsular] cataract may be mediated in part by glucose intolerance and insulin resistance, even in the absence of clinical diabetes” (Weintraub 2002). Several subsequent studies corroborated these findings:

  • In an analysis of nearly 3600 people 49 or older, fasting glucose levels above 108 mg/dL were associated with a 79% greater risk of cortical cataract development over a 10-year period compared to concentrations below 108 mg/dL. Moreover, for each 18 mg/dL increase above this level, risk of progression of some types of cataracts increased by up to 25% (Kanthan 2011).
  • In a similarly designed study on more than 2300 people, fasting glucose levels above 108 mg/dL were associated with a 2.2-fold higher risk of cortical cataracts over a 5-year period (Saxena 2004).
  • Another analysis of 3654 elderly subjects in Australia showed that glucose concentrations between 108 and 126 mg/dL were predictive of doubled risk of cortical cataracts over a 10-year period (Tan 2008).

Interventions associated with improved glucose control have been shown to reduce cataract risk. For example, in an animal model of cataracts, caloric restriction, that is, the reduction of calorie intake to a level short of malnutrition, was associated with a 27% reduction in glucose levels, fewer incidence of cataracts, and less cataract progression (Taylor 1995). Other animal studies showed that use of the anti-diabetic drug acarbose, which inhibits carbohydrate absorption and suppresses glucose concentrations, both reduced incidence and lessened progression of cataracts (Madar 1993, 1994; Cohen-Melamed 1995).

The dangers posed by impaired fasting glucose concentrations are, sadly, often underappreciated by the medical establishment (Jessani 2009). Conventional physicians, in many cases, fail to take preventive action until clinical diabetes manifests, which is defined as fasting blood glucose levels of 126 mg/dL or higher (Aoki 2007; Drexler 2001). In order to avert unnecessary disease, Life Extension® suggests that most individuals strive for an optimal fasting blood glucose level of 80 – 86 mg/dL. More information about glucose control is available in Weight Loss protocol.

9 Nutrients

Antioxidant Protection

Glutathione.  Since glutathione is present in very high concentrations in the lens and is essential for lens transparency, it is an important endogenous antioxidant molecule in the lens (Giblin 2000). Glutathione directly scavenges reactive oxygen species and free radicals, preventing the oxidation of structural proteins in the lens; this is particularly important in several types of cataracts, where oxidative damage to lens proteins appears to play a key role (Kamei 1993; Boscia 2000).  After scavenging reactive oxygen species and free radicals, the oxidized form of glutathione is readily recycled by a specialized enzyme (Lou 2003). As we age, the recycling of glutathione decreases progressively, the pool of reduced glutathione decreases, and oxidized forms of glutathione begin to build up (Xing 2010). This is especially true in the center of the adult lens, known as the nucleus, where even small amounts of UV exposure can drive free radical formation and the generation of cataracts (Giblin 2000; Spector 1995). Nutrients currently taken by most Life Extension customers, such as N-acetylcysteine, lipoic acid, melatonin, and selenium, naturally increase glutathione activity in the body (Atkuri 2007; Jariwalla 2008; Limon-Pacheco 2010; Jiang 2012).

Vitamin C.  Also known as ascorbic acid, vitamin C provides extra antioxidant support in the lens by acting as a “sink” for ROS and free radicals. Its oxidized form, dehydroascorbic acid, is then converted back to ascorbic acid by glutathione and indirectly in reactions that depend on glutathione (Giblin 2000; Lou 2003; Michael 2011). Therefore, vitamin C and glutathione are thought to work together to promote proper water balance within the lens and prevent protein clumping.

The importance of vitamin C for the health of the eye is supported by the finding that vitamin C concentrations in the lens are 20-30 times higher than those in the plasma (Ravindran 2011). In addition, its importance is supported by experiments showing that inhibitors of the enzyme that recycles glutathione cause a marked increase in dehydroascorbic acid, and that dehydroascorbic acid can cause loss of transparency in the lens in animals if it is not converted back into vitamin C (Giblin 2000; Michael 2011). A study examining the effect of long-term dietary supplementation with vitamin C in women showed that supplementation over 10 years significantly decreased the incidence of early age-related cataracts at any location in the lens. Importantly, this study excluded women previously diagnosed with cataracts, to make sure that those who started vitamin C supplementation at the recommendation of their doctors, and as a result of their diagnoses, were not included (Jacques 1997). Another study, which included a large number of men and women, revealed that high consumption of vitamin C, alone or together with other antioxidants (vitamin E, beta-carotene, and zinc), protected against the development of nuclear cataracts (Tan 2009). A study that enrolled over 4000 participants reported that for every 1 mg/dL increase in vitamin C in the serum, there was a 26% decrease in cataracts (Simon 1999). Additionally, in a study in India that enrolled over 5600 individuals, a strong association was found between high serum vitamin C levels and low incidences of cataract (Ravindran 2011).

Vitamin B2.  Also known as riboflavin, vitamin B2 is a vital component of flavin adenine dinucleotide (FAD). FAD, which is directly involved in breaking down carbohydrates and lipids, is important for proper cellular energy balance, and is also used by the enzyme that recycles glutathione back into its bioactive form. It was shown in several animal models that deficiency of dietary riboflavin can lead to cataracts (Bunce 1990). Several studies in humans reported that riboflavin is important in preventing the formation of cataracts. In one study, women with the highest dietary riboflavin intake, as compared to those with the lowest intake, had a lower risk for cataracts (Mares-Perlman 1995). Another study reported that individuals with the highest dietary riboflavin intake had an approximately 50% lower risk of developing cataracts (Cumming 2000).

Vitamin E. Vitamin E naturally occurs in eight different chemical forms, including alpha-tocopherol and gamma-tocopherol (Albanes 1996; MayoClinic 2012). It possesses distinct antioxidant properties and prevents the accumulation of free radicals produced during fatty acid breakdown. Since it is fat-soluble, vitamin E protects fatty tissues and cellular membranes by neutralizing free radicals and ROS. One study among women revealed that those with the highest intake of vitamin E from food and supplements had a 14% lower risk of cataracts (Christen 2008). Another study that examined participants 40–79 years old revealed lens opacities were more frequent in people with lower vitamin E levels (Leske 1995). Yet another study showed that the level of total tocopherol, which is the sum of the serum alpha-tocopherol and gamma-tocopherol, was associated with a decreased risk of developing cataracts (Lyle 1999).

Lipoic acid. Evidence suggests the potent antioxidant lipoic acid may help prevent diabetic cataract formation (Packer 1995; Maitra 1996; Kojima 2007). Since it is distributed in fat-soluble and water-soluble areas of cells and tissues, lipoic acid neutralizes a variety of free radicals (Bast 1988; Packer 1995). Lipoic acid exists in two forms: R-lipoic acid and S-lipoic acid. Of these two, R-lipoic acid in isolation was shown to prevent cataract formation (Maitra 1996). The higher efficacy of R-lipoic acid as compared to alpha-lipoic acid, which is a mixture of both forms, may be related to the higher rate of R-lipoic acid absorption by the lens.

N-acetylcysteine. N-acetyl-L-cysteine (NAC), which is a powerful antioxidant and derivative of the amino acid cysteine, has been shown to prevent opacification in the lens (Wang 2009). NAC also supports the production of glutathione (Pizzorno 1999; Zafarullah 2003; Radtke 2012). By combining NAC with diallyl disulfide, a major organosulfide found in garlic oil, researchers discovered that the latter could boost the antioxidant properties of the former, and the combination prevented the formation of cataracts (Zhao 1998). In animal models, NAC has been shown to prevent lens opacification and inhibit cataract formation (Wang 2009; Carey 2011). Another study found that the combination of NAC and glutathione ethyl ester (GSH-EE), administered as eye drops, slightly inhibited the progression of diabetic cataracts at early stages in rats (Zhang 2008).

Melatonin.  Melatonin, a naturally occurring hormone, has been shown to reduce oxidative stress in the lens and protect against cataract formation (Yaqci 2006; Taysi 2008). Although the mechanism(s) involved have yet to be determined, the increased production of glutathione or direct scavenging of free radicals are thought to be involved (Abe 1994). Given that melatonin levels decline with age, and in light of the rising incidence of cataracts in the latter part of life, melatonin supplementation may be useful for cataract prevention among aging individuals (Abe 1994).

Combating Glycation Reactions and Protecting Lens Structure and Function

Carnosine. Carnosine, along with one of its derivatives N-acetyl-carnosine, is a potent inhibitor of glycation reactions and oxidative damage; it has been shown to efficiently penetrate the lens (Hipkiss 2000; Babizhayev 2012; Wang 2000). Like glutathione, carnosine levels decrease with age (Bellia 2009; Everaert 2011). At moderately high concentrations, carnosine was able to attenuate UV-induced aggregation of lens proteins (Babizhayev 2009). When delivered topically as eye drops twice daily, a solution of N-acetyl-carnosine has been shown to delay onset of diabetes-induced cataracts (Attanasio 2009; Shi 2009;). 

N-acetyl-carnosine eye drops have also been shown to be effective in dogs. Visual improvements were reported in 80% of the participating dogs administered eye drops containing N-acetyl-carnosine (Williams 2006). Taken together with information from human trials and experiments in rodents, it appears that N-acetyl-carnosine eye drops may offer considerable protection against the formation and progression of cataracts (Quinn 1992; Attanasio 2009; Babizhayev 2009; Shi 2009).

Carnitine and Acetyl-L-Carnitine. Carnitine is a naturally occurring, amino acid-like compound found in all mammals with essential roles in normal function of the mitochondria, the energy powerhouses of cells; its derivative, acetyl-L-carnitine, is a powerful antioxidant and has been shown to combat glycation reactions (Reuter 2012; AMR 2010; Swamy-Mruthinti 1999). An examination of extracted human cataractous lenses showed that as opacification increased, carnitine concentrations decreased, with lenses containing the greatest opacification having about 30% lower carnitine concentrations than those with the least opacification (Gawecki 2004). In an animal model of cataracts, acetyl-L-carnitine strongly inhibited chemical-induced cataractogenesis. The researchers attributed the effects of acetyl-L-carnitine to its role as an antioxidant within the lens (Elanchezhian 2007). In a subsequent study, researchers from this same group showed that acetyl-L-carnitine also guards against “self-destruction”, or apoptosis of lens cells (Elanchezhian 2010). Evidence also indicates acetyl-L-carnitine protects against cataract development subsequent to ionizing radiation exposure by upregulating intrinsic antioxidant defense mechanisms (Kocer 2007).

Bioflavonoids.  Bioflavonoids, a class of plant-derived molecules with antioxidant properties, that may be beneficial in cataracts by helping combat the accumulation of water within lens cells, which disrupts normal light refraction (Head 2001; Matsuda 2002). Specifically, the bioflavonoid quercetin, the most widely consumed flavonoid in the human diet, was shown to inhibit diabetic cataract development, possibly acting on multiple pathways, and maintain the transparency of the lens in response to oxidative stress (McLauchlan 1997; Stefek 2011). Another animal experiment showed that quercetin helped maintain lens transparency by balancing calcium, sodium, and potassium ions within the lens (Ramana 2007).

Vitamin B6. Vitamin B6, or pyridoxine, is an important water-soluble cofactor necessary for the metabolism of amino acids and the synthesis of nucleic acids required for DNA replication and repair. It has been shown to significantly reduce the production of AGEs in the diabetic lens (Jain 2002; Padival 2006). Though human studies in cataract patients still need to be conducted, a trial in which vitamin B6 and vitamin B1 were administered to diabetic patients showed the combination significantly inhibited DNA glycation in white blood cells, suggesting systemic benefit (Polizzi 2012).

Additional Support for Healthy Eyes

Carotenoids.  Carotenoids, a type of pigment found in plants, absorb light and safeguard against the oxidative effects of UV rays. Several carotenoids, including lutein, zeaxanthin and meso-zeaxanthin are not only present at high levels in the retina, but also help prevent cataract formation and macular degeneration (Arnal 2009; Gao 2011; Kijlstra 2012). A study on a large group of women, ages 45–71, revealed that dietary lutein and zeaxanthin, and foods rich in these carotenoids, reduced the risk of cataracts that were sufficiently severe to require surgery (Chasan-Taber 1999). Another large study that enrolled people >40 years old found that those with a high dietary intake of lutein and zeaxanthin had a lower risk for nuclear cataracts (Vu 2006). In another study on 1802 women, subjects in the highest quintile (one-fifth) of distribution for blood levels or dietary intake of lutein and zeaxanthin were 32% less likely to have nuclear cataract compared to women in the lowest quintile (Moeller 2008). In a small double-blind, randomized clinical trial on 17 patients with cataracts, supplementation with lutein (15 mg, 3 times weekly for up to 2 years) was associated with improved visual acuity (Olmedilla 2003).

Bilberry.  Bilberry is rich in anthocyanins, which are plant pigments that exert a variety of beneficial effects in the human body, including functioning as antioxidants and modulating inflammatory processes (Tsuda 2012; Karlsen 2010). Importantly, these anti-inflammatory and antioxidant effects were observed within the eye in an animal model (Miyake 2012). In an experimental model involving animals prone to age-related eye diseases such as macular degeneration and cataracts, long-term administration of bilberry extract completely abrogated impairments in the lens and retinas, whereas 70% of control animals developed cataract and macular degeneration (Fursova 2005). Bilberry has yet to be studied in large trials to assess its effects on cataracts in humans, but controlled studies have found benefits associated with bilberry supplementation, alone or in combination with other nutrients that support eye health, for eye strain and glaucoma (Kawabata 2011; Shim 2012).

Green tea and back tea. Green and black teas contain antioxidant molecules called catechins and polyphenols, which have been studied in many human health conditions (Singh 2011; Miyazawa 2000; Kerio 2013). Several animal studies show that green and/or black tea can mitigate cataract formation or progression. In one such study on rats with chemical-induced diabetes, green and black teas, administered in drinking water, were shown to retard cataract development by reducing the detrimental effects of elevated glucose on the lenses (Vinson 2005). Another study found that green tea extract bolstered antioxidant defenses and reduced the incidence of chemical-induced cataracts in an animal model (Gupta 2002). A similar study on an animal model of chemical-induced cataracts revealed that green and black tea extracts slowed progression of lens opacification (Thiagarajan 2001).

Resveratrol. Resveratrol, a natural polyphenol found in several plants (including grapes, peanuts, and pines), has multiple health benefits due to its function as an antioxidant (Zheng 2010). In an animal model of chemically-induced cataracts, resveratrol was shown to reduce oxidative stress in the lens and suppress cataract formation (Doganay 2006). Resveratrol was also able to increase the survival of human lens epithelial cell cultures that were subjected to oxidative stress, and it decreases the cellular markers of aging (Li 2011). These effects could be explained by its ability to increase the activity of intrinsic antioxidant enzymes – superoxide dismutase, catalase, and heme oxygenase (Zheng 2010).

Selenium.  Selenium is a trace mineral involved in many biologic functions within the human body. Studies have shown that selenium can slow the development of cataracts by lowering oxidative stress in the lens (Zhu 2012). Although additional studies are required to determine how selenium prevents oxidative damage in the lens, it has been shown to enhance recycling of glutathione (Chada 1989; Baker 1993).

Vitamin K. Vitamin K is a fat-soluble vitamin found in leafy greens such as spinach and collard greens. Phylloquinone, or vitamin K1, is the primary source of vitamin K in the diet (Booth 2012). Vitamin K1 has been shown to inhibit the enzyme aldose reductase, which converts glucose into sorbitol, a sugar alcohol. Accumulation of sorbitol in the eye lens contributes to the pathogenesis of cataracts (Murata 2001; Thiagarajan 2019). Preventing accumulation of sorbitol and its degradation product, fructose, in the lens decreases free radical stress and lessens osmotic pressure, decreasing the risk of cataract formation (Sai Varsha 2014; Thiagarajan 2019). A retrospective analysis of a large randomized controlled trial found that greater dietary vitamin K1 intake was associated with lower cataract risk. The trial enrolled 5,860 Mediterranean people and assessed dietary vitamin K1 intake via a food questionnaire. After nearly six years of follow-up, participants who consumed the highest levels of vitamin K1 had a 29% lower risk of developing cataracts than those with the lowest intake levels (Camacho-Barcia 2017).


  • Oct: Added section on vitamin K to Nutrients


  • Mar: Comprehensive update & review

Disclaimer and Safety Information

This information (and any accompanying material) is not intended to replace the attention or advice of a physician or other qualified health care professional. Anyone who wishes to embark on any dietary, drug, exercise, or other lifestyle change intended to prevent or treat a specific disease or condition should first consult with and seek clearance from a physician or other qualified health care professional. Pregnant women in particular should seek the advice of a physician before using any protocol listed on this website. The protocols described on this website are for adults only, unless otherwise specified. Product labels may contain important safety information and the most recent product information provided by the product manufacturers should be carefully reviewed prior to use to verify the dose, administration, and contraindications. National, state, and local laws may vary regarding the use and application of many of the therapies discussed. The reader assumes the risk of any injuries. The authors and publishers, their affiliates and assigns are not liable for any injury and/or damage to persons arising from this protocol and expressly disclaim responsibility for any adverse effects resulting from the use of the information contained herein.

The protocols raise many issues that are subject to change as new data emerge. None of our suggested protocol regimens can guarantee health benefits. Life Extension has not performed independent verification of the data contained in the referenced materials, and expressly disclaims responsibility for any error in the literature.

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