Life Extension Magazine

Life Extension Magazine 2010

Report

Cutting-Edge Berry Extract For Improved Night Vision

By Kirk Stokel

By Kirk Stokel

In terms of personal safety, getting behind the wheel of a car can be a risky endeavor. But driving a car at night is even riskier.

Almost half of all fatal car crashes in the US occur at night.1 Nearly half of all aviation fatalities also take place at night, even though only 7% of all flights are night flights.2

The reason is simple. Humans did not evolve the capacity to see well in poorly lit conditions. As we age, our night vision ability plummets.

For example, falls are the number one cause of serious injuries in older people, accounting for 70% of accidental deaths.3 Darkness is often the culprit.

Fortunately, cutting-edge researchers have identified a nutrient that not only improves vision—but has the power to regenerate the molecules in your eyes that help you see in darkness.

This next-generation nutrient, called cyanidin-3-glucoside or C3G, is found in high concentrations in certain berries native to Europe.

In a clinical study on the effects of a concentrated berry extract containing C3G, a group of aging individuals taking just 50 mg experienced improvement in their ability to see in darkness after just 30 minutes!4

In this article, you will learn how this novel plant-based nutrient acts in multiple ways to enhance eyesight and nourish the structures you need to see in dim-light conditions. You will also find out how an international research team recently established C3G’s pharmacologic power to improve eyesight at night.

A Breakthrough Discovery: Vision Regeneration

A Breakthrough Discovery: Vision Regeneration

As we age, our ability to see in the dark is impaired. The reason is that a compound in our eyes called rhodopsin (which absorbs light in our retina) dramatically declines over time.

Aging is directly associated with a reduction in the ability of rhodopsin to regenerate, resulting in progressive loss of dark vision.5

Researchers have discovered a novel solution to the problem of declining night vision called C3G, which is short way of saying cyanidin-3-glucoside.

C3G is a purple pigment in the anthocyanin family of flavonoid molecules. It is found in highest concentrations in dark fruits like blackberries and black currants.6,7 Like most flavonoids, it is a powerful antioxidant8—a critical protective factor in the high-energy environment of the retina, where continuously flowing electrons and photons produce damaging free radical surges.9

C3G is a purple pigment in the anthocyanin family of flavonoid molecules. It is found in highest concentrations in dark fruits like blackberries and black currants.

Scientific Studies on C3G and the Eye

As early as 2003, Japanese researchers discovered that C3G stimulated rhodopsin regeneration in animal retinal cells.10 These findings were extended with two landmark papers in 2009. The first showed that C3G binds directly to rhodopsin in both its dark- and light-adapted states.11

The second study showed that C3G binding creates a beneficial change in the molecular structure of rhodopsin.12 Remember that rhodopsin is the complex in your retina that absorbs light.

By opening up the binding site for a pigment known as retinal, C3G speeds the regeneration of rhodopsin. It’s that rapid regeneration of rhodopsin that makes C3G so exciting to vision scientists for its potential to enhance night vision.

A supportive study involving a group of healthy volunteers found that just 50 mg of a berry extract concentrate containing C3G helped aging individuals to see better in darkness after 30 minutes.4

Scientific Studies on How C3G Benefits Other Tissues

Scientific Studies on How C3G Benefits Other Tissues

Interestingly, C3G, which is highly bioavailable, enhances other functions in the body.13-15 Its potent antioxidant properties protect tissues against DNA damage, often the first step in cancer formation and aging of tissues.16,17

C3G protects endothelial cells against peroxynitrite-induced endothelial dysfunction and vascular failure.18 In addition, C3G fights inflammation by inhibiting inducible nitric oxide synthase (iNOS), reducing vascular inflammation.19 At the same time C3G upregulates activity of endothelial nitric oxide synthase (eNOS), which helps maintain normal vascular function.20 These effects on blood vessels are especially important in the retina, where delicate nerve cells depend on the single ophthalmic artery for their sustenance.

In animal models, C3G prevents obesity and ameliorates blood sugar elevations.21 One way it does this is by increasing gene expression of the beneficial fat-related cytokine adiponectin.22 As we well know, diabetics are predisposed to severe eye problems including blindness from elevated blood sugar levels.

C3G helps to induce apoptosis (programmed cell death) in a number of human cancer lines, an important step in cancer prevention.23,24 In a similar fashion (but via a different mechanism), C3G stimulates rapidly proliferating human cancer cells to differentiate so that they more closely resemble normal tissue.25

Finally, in early 2010, it was discovered that C3G is neuroprotective, helping to prevent the disastrous effects of the Alzheimer’s-related protein amyloid beta on brain cells.26

C3G acts at multiple targets throughout the body to protect vision. To achieve maximum eye protection, C3G works in concert with other nutrients that guard eyes from the many age-related threats to vision.

Protecting the Macula

Up until middle age, our retinas are protected from the onslaught of severe damage from intense sunlight. We owe the natural light protection in our youthful retinas to a group of plant-derived molecules called carotenoid xanthophylls. The retina contains 3 kinds of carotenoids, of which two, lutein and zeaxanthin, predominate.27

With the addition of meso-zeaxanthin (which in young eyes is formed from lutein), these carotenoids account for the “yellow spot” at the macula.28,29

Protecting the Macula

The macula is the part of the retina on which most light falls, and is therefore most vulnerable to light-induced damage.29 It’s no coincidence that carotenoids are concentrated in the macula: their yellow pigment is a function of their molecular structure, which allows them to avidly absorb the blue light that is most destructive to retinal cells.30,31 These pigments also have powerful antioxidant properties, helping them rapidly quench oxygen free radicals produced by photons striking retinal tissue.29,32

But macular pigments decline with age, leaving the retina increasingly unshielded from harsh radiation. In fact, as pigment levels drop, the incidence of age-related macular degeneration increases.

Macular degeneration is the leading cause of blindness in the elderly.31 Because it destroys vision in the center of the visual field, macular degeneration has a tremendous impact on one’s ability to recognize faces, to drive, and to read, contributing to the growing isolation that’s so devastating to elderly people.33

Sadly, the average intake of carotenoid pigments in the US is below the levels known to afford protection from eye disease.34 There’s compelling evidence that dietary deficiencies in these nutrients contribute to eye diseases such as macular degeneration and cataracts.35,36 Fortunately, there’s equally unequivocal evidence that supplementation offers protection.36 Let’s take a look.

It’s been known for years that higher dietary intakes of lutein and zeaxanthin were associated with decreased likelihood of age-related macular degeneration.37 More recently, higher blood levels of carotenoids were found to be associated with preventing cataracts as well.38,39 But simply increasing one’s intake of fruits and vegetables rich in these pigments, while beneficial for overall health, has failed to affect the concentration of carotenoids in the retina.40 To do that, supplementation is required.

Protecting the Macula
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The large Lutein Antioxidant Supplementation Trial (LAST) was designed to determine the effects of supplementation on density of macular pigments in people with age-related macular degeneration.41 Subjects received 10 mg lutein alone; lutein with vitamins, minerals, and antioxidants; or a placebo. The density of macular pigment increased in both supplemented groups, and declined significantly in the placebo recipients. Most vitally, this study established that people with the lowest pigment density (and therefore in greatest need of supplementation), obtained the greatest benefit from supplementation. The authors concluded that “If a deficiency in macular pigment optical density is accurately diagnosed, effective interventions should be able to re-establish this prophylactic barrier.”41

A study by Italian ophthalmologists advanced our knowledge by an additional step.42 Studying people with early age-related macular degeneration, they demonstrated a remarkable increase in the electrical response to light of subjects’ retinas following supplementation with lutein 10 mg, zeaxanthin 1 mg, and astaxanthin 4 mg, along with antioxidant vitamins and minerals. This was the first study to show that supplements improve retinal function.

Protecting the Macula

Numerous other studies have confirmed and elaborated on these results. Lutein in combination with docosahexaenoic acid (DHA from fish oil) provided an increase in pigment density evenly throughout the retina.43 A 2010 trial demonstrated increased macular pigmentation, especially in the crucial central portion of the retina, after just 2 weeks of supplementation with lutein, zeaxanthin, and meso-zeaxanthin.44 The combination of lutein plus zeaxanthin provides the best coverage of pigment in both central and peripheral areas of the retina.45 Supplementation with lutein, zeaxanthin, and black currant extract has also been shown to reduce symptoms of visual fatigue, a common problem with advancing age.46

Cataracts are another leading cause of vision loss in older adults, and one we now know may be preventable with supplementation. People with higher intakes of lutein and zeaxanthin are at decreased risk for cataracts.39,47,48 Laboratory studies demonstrated that lutein inhibits changes that contribute to cataracts in both normal and diabetic eyes.49,50 Finally, lutein supplements improved visual function in people with age-related cataracts.51

Unique Mechanisms of Meso-zeaxanthin and Astaxanthin

While lutein and zeaxanthin are the main xanthophylls in the retina, lutein is also transformed into meso-zeaxanthin in the retina itself.31 Meso-zeaxanthin is found only in a few foods, such as shrimp shells and fish skin—hardly appealing sources for this valuable nutrient.27 Fortunately, meso-zeaxanthin is readily absorbed into the blood following oral supplementation, and it contributes significantly to improving macular pigment density when used as a supplement.

Light not only depletes the retina of protective pigments, it also induces powerful oxidant stresses that result in inflammatory responses in both retina and lens. Another xanthophyll, the red pigment astaxanthin, provides comprehensive protection against these threats.52,53 In fact, astaxanthin in combination with lutein and zeaxanthin protected human lens tissue from ultraviolet light damage better than vitamin E.54

Cataracts are another leading cause of vision loss in older adults, and one we now know may be preventable with supplementation.

Inflammatory changes in the retina contribute to long-term retinal damage, mostly through their impact on the health of tiny blood vessels within the eye. Astaxanthin reduces inflammation in the eye by the following mechanisms:

  • Suppresses the pro-inflammatory signals inducible nitric oxide synthase (iNOS), prostaglandin E2, and TNF-alpha.55
  • Downregulates the vital signaling pathway controlled by nuclear factor-kappaB, which controls cellular responses to inflammation.56
  • Protects DNA from damage induced by reactive nitrogen species as well.57

Astaxanthin’s anti-inflammatory effects also protect retinal tissue from so-called “wet” age-related macular degeneration by reducing the formation of new blood vessels seen in advanced disease.58 Finally, astaxanthin protects retinal cells from dying as the result of the increased pressure within the eye that characterizes glaucoma, another tragic cause of blindness in the elderly.59

Summary

Nearly half of all automobile and aviation fatalities occur at night. Dim-lighting conditions are a major factor in falls, the leading cause of accidental death in older persons. This horrific death toll stems primarily from the fact that human beings did not evolve the capacity to see well in darkness.

Researchers have recently uncovered the power of berry flavonoid compounds such as cyanidin-3-glucoside or C3G to optimize eyesight and enhance night vision. It favorably affects molecular processes that speed restoration of the eye pigment rhodopsin—the primary catalyst for optimized night vision. (See sidebar below for details.)

Lutein, zeaxanthin, and meso-zeaxanthin help protect retinal and lens tissue from light damage, helping to prevent macular degeneration and cataracts. Astaxanthin provides additional protection against inflammatory changes that can worsen macular degeneration, as well as against elevated pressure from glaucoma.

These nutrients provide benefits to cells throughout the body.

If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at
1-866-864-3027.

Rhodopsin and the C3G Breakthrough: How It Works
Unique Mechanisms of Meso-zeaxanthin and Astaxanthin

C3G’s optimizing mechanism of action on night vision—first detected by a team of Japanese researchers in 2003—ultimately “came to light” in 2009, when they were finally able to outline in detail how C3G works.

Under normal visual conditions, we perceive light when photons (light particles) pass through the lenses of the eye and fall on the retina. The eye evolved to receive and process light into images through two types of structures in the retina called photoreceptors—rods and cones, specifically. Cones perceive light, while rods are highly sensitive to darkness.

Rhodopsin is the protein complex responsible for night vision. It’s used specifically by the dark-responsive rods.60 When a molecule of rhodopsin absorbs a photon, it splits into a retinal molecule (11-trans-retinal) and an opsin molecule.61 This molecular breakdown of rhodopsin initiates a biochemical-to-electrical reaction that sends signals to the visual processing center of your brain, allowing you to make out images in the dark.62 Retinal and opsin then recombine into rhodopsin.

Although the splitting of rhodopsin into retinal and opsin is virtually instantaneous, it can take tens of minutes for opsin and retinal to reconstitute and restore rhodopsin to optimal levels.63

During that interval, your ability to see in the dark is impaired (think about what happens when you step into a dark room after being out in direct sunlight). Aging is directly associated with a reduction in the ability of rhodopsin to regenerate, resulting in progressive loss of dark vision.5

C3G accelerates the recombination of retinal and opsin into rhodopsin, enabling the rods responsible for night vision to resume functioning much faster. The result? Precious extra minutes to see in dark conditions, whether you’re driving on the road at night or going up a dimly lit flight of stairs.

The evolution of digital cameras is a good analogy. The earliest models took a long time to refresh their memory before you could take another shot. This was frustrating—you had to wait to take another picture, missing other photo opportunities while you waited. But as their processors got faster, digital cameras advanced to the point where you could take multiple pictures instantly—even shoot short videos.

C3G acts similarly on the retina. By recycling rhodopsin faster, C3G works like a graphics accelerator for the eye, allowing more information to be processed faster through the retina in darkness. This sends a greater number of visual “snapshots” to the brain in dim-light situations—snapshots that can make the difference between safety and disaster.

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