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Astaxanthin and eye fatigueWhen using computers more and more in our everyday life – eye fatigue has become a much more prevalent problem than before. When we researched our Anti-Aging Supplement we came across and anti-aging compound that not only makes you look younger, but one of its other positive effects is also that it helps to reduce eye fatigue and asthenopia. To look at the clinical data of how astaxanthin helps your eyes then please read this page.
This page will help explain why astaxanthin helps to reduce inflammation, reduce eye fatigue and how it helps with “eye accommodation” – which refers to the refractive power of the eye to focus objects at different distances. on this page
© Fuji Health Science and various patents and clinical references Eye fatigue and visual display terminals
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| Figure 1. Location of the ciliary body in the human eye
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Some might argue that asthenopia is non-life threatening or disabling compared to age-related macular degeneration, and there is no conclusive evidence suggesting that VDT work damages the eye e.g., advancing myopia; nevertheless this phenomenon contributes to the functional discomfort that greatly affects the quality and performance at work and leisure.
Asthenopia otherwise called eye fatigue occurs on a daily cycle, in that the visual performance generally decreases naturally from morning until night. This problem exacerbates with a daily VDT load that lasts between 4 to 7 hours by affecting the accommodation performance of the ciliary body, which controls lens refraction. A couple of randomized double blind placebo controlled pilot studies demonstrated the positive effects of astaxanthin supplementation on visual function. For example, a study by Nagaki et al., (2002), demonstrated that subjects (n=13) who received 5 mg astaxanthin per day for one month showed a 54% reduction of eye fatigue complaints (Figure 2). In a sports vision study led by Sawaki et al., they demonstrated that depth perception and critical flicker fusion had improved by 46% and 5% respectively on a daily dose of 6 mg (n=9). The effect of astaxanthin on visual performance prompted a number of other clinical studies to evaluate the optimum dose and identify the mechanism of action.
| Figure 2. VDT Subjects with Eye Strain Symptoms before and after astaxanthin supplementation (Nagaki et al.,2002)
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A study by Nakamura (2004), demonstrated significant improvements in reducing asthenopia and positive accommodation for the 4 mg (p<0.05) and 12 mg (p<0.01) groups. However, it was not until Nitta et al., (2005), who established the optimum daily dose at 6 mg (n=10) for a period of 4 weeks by comparing eye fatigue using a visual analogue scale (VAS) based questionnaire and accommodation values. Overall, the 6 mg group improved significantly better at week 2 and 4 of the test period. Furthermore, results obtained by Shiratori et al., (2005) and Nagaki et al., (2006), also confirmed the previous findings that astaxanthin supplementation at 6 mg for 4 weeks improved symptoms associated with tiredness, soreness, dryness and blurry vision. Another study by Takahashi & Kajita (2005), also demonstrated that astaxanthin attenuates induced-eye fatigue, as opposed to treating eye fatigue, which suggests prevention rather than treatment. Astaxanthin treated groups (asthenopia negative) were able to recover quicker than the control group after heavy visual stimulus.
Since the questionnaires may be subjectively limited, the direct measurements of parameters associated with asthenopia are better indicators. These include accommodation amplitude (Figure 3); rate of accommodation reaction (positive and negative directions); CFF (visual central nervous system activity) and PVEP (ophthalmic neural conductivity). Based on the information available, the accommodation related measurements consistently improved after the treatment period (Nagaki et al., 2002, 2006; Nakamura et al., 2004; Takahashi & Kajita, 2005; Shiratori et al., 2005; Nitta et al., 2005) whereas the CFF and FVEP remained inconclusive (Sawaki et al., 2002; Nagaki et al., 2002; Nakamura at al., 200). Therefore, the mechanism by which astaxanthin improved eye fatigue strongly indicates accommodation.
| Figure 3. Objective accommodation (Nitta et al., 2005)
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Accommodation measures the lens refractive property as it corresponds to the ciliary body function. This small ocular muscle controls the lens thickness in order to focus the light on the retina. In heavy visual workloads, the eye is focused on a fixed object distance for extended periods that will cause muscle spasms or develop fatigue detectable by accommodation tests. These tests are interrelated and include the following: accommodation amplitude; accommodation reaction (positive or negative) and high frequency component (HFC). Each clinical study used a combination of accommodation tests to indicate the amount of fatigue present. For example, increased accommodation amplitude in all treated subjects indicated improved reaction on near and far objects (Nagaki et al., 2002, 2006; Nakamura et al., 2004). Figure 4 and Figure 5 reveal the higher rate of accommodation reactions measured in astaxanthin treated groups. These indicate the speed at which the ciliary body reacted to the direction change of focus (positive means from a near object at 35 centimeters to distant object at 5 meters or vice versa); (Nitta et al., 2005; Shiratori et al., 2005; Nakamura et al., 2005).
| Figure 4. Positive accommodation change (Shiratori et al., 2005)
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| Figure 5. Negative accommodation (Shiratori et al., 2005)
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The effects of astaxanthin are significant from 2 weeks. Another technique called HFC directly measured the microfluctuations in the lens during the accommodation response and typical values exist between 50 and 60 for normal eyes. Asthenopia sufferers (values greater than 60) experienced faster rates of recovery (Figure 6) in that their HFC results decrease towards normal values in less time compared to control groups (Takahashi & Kajita, 2005).
| Figure 6. Accommodative Recovery observing difference of HFC (Takahashi and Kajita, 2005)
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Another randomized placebo controlled study by Nagaki et al., (2005) detected the increase of retinal blood flow in the astaxanthin treated group that received 6 mg for 4 weeks (n=14, p<0.01). Even though the precise reason for accommodation improvement seen with astaxanthin is not yet clear, the author postulated that based on the rheological improvement measured in the retinal capillary vessels, most likely means more blood also reaches the ciliary body and provides more nourishment to the ciliary muscles. Furthermore, the rheological improvement agreed with Nagaki et al., (2005) who studied ten healthy subjects treated with 6 mg astaxanthin for ten days (Figure 7). The blood exhibited significantly higher flow rates (ex-vivo) compared to the control group (p<0.05) utilizing the micro-array channel flow analyzer (MC-FAN).
| Figure 7. Increase of retinal blood flow (Nagaki et al., 2005)
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Lastly, a top Japanese ophthalmology research collaboration between Hokkaido, Yokohama and Tokyo concluded anti-inflammatory properties of astaxanthin in endotoxin-induced uveitis (EIU or eye inflammation) both in vivo and in vitro models. Ohgami et al., (2003) observed in a dose dependant fashion that astaxanthin doses of 1, 10 or 100mg/kg dose in rats had the same anti-inflammatory action as 10 mg/kg prednisolone (n=8, p<0.01). Inflammation markers such as nitric oxide synthase (NOS), prostaglandin E2 (PGE2) and tumor necrosis factor (TNF)-a were all significantly reduced. In human terms, 4 mg astaxanthin per day may deliver the same benefits as 4 mg prednisolone without the side effects of intraocular pressure build-up. Other reduced biomarkers were cellular infiltration and protein build up in the aqueous humor.
In another study, Suzuki et al., (2006) confirmed the same effects while they carefully studied the anti-inflammatory effect of astaxanthin in the iris-ciliary body of rat eyes. This was also the first study to prove that astaxanthin suppressed NF-kB activation by free radicals in the EIU rat model (Figure 8). The result is a lower pro-inflammatory response that would otherwise perpetuate local sites of inflammation that may also help explain why astaxanthin worked to alleviate eye fatigue in numerous clinical trials.
| Figure 8. Number of NF-.B positive cells in eye ciliary body during inflammation (Suzuki et al., 2006)
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For astaxanthin to work, it has to pass through the human blood-retinal barrier (BRB) for which there is no direct evidence because a non-invasive specific quantification method is not available. However, the BRB is a selective barrier similar to the blood-brain barrier (BBB), which is better understood, so astaxanthin is expected to pass through because of the molecular size, is less than 600 Daltons. Furthermore, astaxanthin belongs to the same carotenoid xanthophyll group as lutein and zeaxanthin, both of which are concentrated in the macular region of the eye. Unlike, beta-carotene or lycopene (carotenes), xanthophylls are the only carotenoids detected in the eye so far.
Eye fatigue or asthenopia is a common problem that occurs with the regular use of VDTs and may be resolved with findings from many worldwide epidemiological studies. However, if current improvements tend to be only 50% successful and other factors are likely to be involved, therefore, based on the current clinical evidence, astaxanthin offers a complementary alternative by reducing inflammation, improving accommodation and increasing blood flow.
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