Chromatic aberration, comprising both longitudinal (LCA) and transverse (TCA) components, has been cited as possibly the most significant aberration affecting visual quality. 10 Indeed, LCA creates up to two dioptres of wavelengthdependent optical defocus. Campbell and Gubbisch 11 have demonstrated improvements in contrast thresholds of up to 65 % at intermediate spatial frequencies once monochromatic yellow light is employed in place of spectrally broadband white light. Although Bradley 12 later modelled the effects of chromatic aberration, and concluded that the effect of chromatic aberration on the modulation transfer function was small, and equivalent to approximately 0.15D of defocus, upper resolution limits of the visual system however, are most likely defined by the effects of chromatic aberration. 13

The effect of LCA across wavelength, in terms of blur, is non-linear, as shorter wavelengths are significantly more defocused than longer wavelengths. For example, an eye focussed at 550nm, light at 460nm suffers 1.2D myopic defocus, while the equivalent long wavelength of 640nm is only 0.50D out of focus. 10 This serves to create a purple blur circle haze around the focussed “green” component. Figure 2 demonstrates the non-linearity of defocus and the relative luminance profile across wavelength. As the spectral extremities have less luminosity, the effects of chromatic aberration on image focus are mitigated in terms of the effects on vision. Mitigation is potentially further aided by the fact that blue light is selectively absorbed by MP.

Figure 2.

Illustration of the relative luminance profile and the effect of chromatic aberra tion across wavelengths. The relative blur is more pronounced at the blue end of the spectrum such that, for example, the short wave 460nm text is significantly more difficult to recognise than the long wave 640nm text for the above scenario where the optimal focus is between 540-560nm.

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If one looks up to the sky on a bright, cloudless sunny day, one could be fooled into thinking that the sun's rays traverse an unobstructed path to the eye. Furthermore, one could certainly not imagine that the quality of the light visible was being degraded as it traversed the seemingly clear sky, even in the most remote countryside locations far from the smog-filled cityscapes, on its way to the eye. The fact that the sky is blue is testament to the impact of the process of light scatter, whereby particle matter abstracts and re-radiates energy from light incident upon it.

A multitude of visible and non-visible particles, varying in size from atmospheric oxygen and nitrogen, to haze aerosols, to larger complexes such as fog, cloud and rain, all contribute to such scatter. Wooten & Hammond, 14 in an excellent review of the importance of light scatter to the “visibility” of objects, eloquently describe why light scatter, especially that induced by haze aerosols “critically determines how far one can see and how well details can be resolved”, so that, aside from the optical and neural limits, “scatter in the aerosol haze is the primary determinant of visual discrimination and range in the outdoors”.

The question therefore arises, what effect does light scatter have on visual performance? And it is a good question. On a clear day one can see for miles despite the effects of scatter. Wooten & Hammond, 14 however, propose a model whereby compensation for the effects of light scatter, such as could reasonably be achieved by increasing the optical density of MP, would increase the visibility and discriminability of targets in natural settings. In their model, a 1 log unit increase in MPOD attenuates the veiling luminance of the short-wave dominant background by 26 % (or 17 % for a more practical 0.5 log unit increase in MPOD), while having minimal effect on the short wave deficient distant target. The attenuation of the effects of light scatter is thereby observed to enhance target detection and discrimination capacity, and extend the visual range by up to 18.6 %.

Tackling the question from another perspective, the problems caused by scatter, while not consciously experienced by most people, do become a significant symptom of which many patients complain in the form of discomfort and disability glare. Aside from patients without detectable ocular abnormality, typical patients with such symptoms include those with cataract, corneal abnormalities, intraocular inflammation, and following laser refractive surgery, amongst others. Therefore, scatter does have an adverse effect on the visual experience of normal subjects and on those with ocular pathology, and any means of alleviating such effects would be of clinical importance.

The possible effect of aberrations such as LCA, and also of short wavelength light scatter, is that capacity limits are somewhat reduced so that the anatomic limits of acuity based on foveal cone diameter (30 seconds arc — equivalent to 6/3) are seldom achieved, even in healthy normal individuals, with the exception of hyperacuity tasks which have different underlying neural bases.

So the question arises, what are the properties of MP that might allow it to improve visual performance in light of the limiting factors outlined above?

Abnormal light sensitivity, difficulty associated with glare, loss of contrast and slow dark adaptation are symptoms commonly reported by patients with hereditary retinal degenerations. It is possible that such symptoms could be attributable, at least in part, to the failure of MP to absorb scattered light, resulting in reduced contrast and definition along with excessive photoreceptor pigment bleaching by short wavelength light components.

The antioxidant and absorptive properties of MP would therefore suggest a potentially useful role for the macular carotenoids in retinal degenerations, where the clinical aim includes optimisation of current visual status in the short term and preservation of macular vision in the long term. Indeed, it is noteworthy that there have been reports (some dating back > 50 years) suggesting that patients with retinitis pigmentosa (RP) demonstrated improvements in visual performance following supplementation with lutein-containing compounds (reviewed elsewhere 16).

Dagnelie et al. 32 assessed the effect of L supplementation in patients with RP, and reported moderate visual improvements following short-term supplementation with L. Mean visual acuity improved by 0.7 dB and mean visual-field area by 0.35 dB, although the largest gains

Duncan et al. 34 analysed MP levels and macular function in choroideremia (a progressive degeneration of photoreceptors, RPE and choroid). Once again, and in spite of augmented MPOD following supplementation, no improvement in retinal sensitivity was observed.

Aleman et al. 35 measured MPOD in patients with Stargardt's disease or cone-rod dystrophy with known or suspected disease-causing mutations in the ABCA4 gene, and investigated response to supplemental L in terms of changes in MPOD and central visual function. They reported that MPOD is inversely related to the stage of ABCA4 disease at baseline, and could be augmented by supplemental L in about two thirds of patients. However, measures of visual function, including visual acuity and foveal sensitivity, exhibited no discernable improvement after 6 months of supplementation. They concluded that the long-term influences of L supplementation on the natural history of such macular degenerations require further study.

AMD, as the leading cause of blindness in the western world, is the most commonly investigated retinal condition with respect to the potential benefits of supplemental L, Z, or meso-Z. Observations, including relative preservation of short wave sensitive cones centrally when compared to the perifoveal region 36 and the initiation of geographic atrophy in the perifovea, where MPOD is lowest, are consistent with the view that MP protects against AMD and against psychophysical changes known to precede this condition. Since publication of the findings of the Eye Disease Case-Control Study Group, where a 60 % risk reduction for AMD in association with a high dietary intake of L and Z was reported, 37 numerous investigators have further explored the relationship between dietary and serum levels of MP's constituent carotenoids and risk for AMD. 38 With a couple of exceptions (outlined below), studies investigating serum levels of, dietary intake of, or supplementation with, L and/or Z with respect to risk for AMD and/or its progression have (understandably) considered preservation, rather than enhancement, of visual performance, to represent the most appropriate outcome measure (reviewed elsewhere 39).

Richer 40 evaluated the effect of dietary modification on visual performance for patients with atrophic AMD. Fourteen male patients (70±9 years), receiving 0.73±0.45 portions of dark-green, leafy vegetables/day base intake, were placed on an additional portion of 5 ounces sautéed spinach 4 to 7 times per week or lutein-based antioxidant (3 subjects). Patients demonstrated short-term enhancement of visual function in one or both eyes in terms of amsler grid testing, Snellen acuity, contrast sensitivity, glare recovery, and subjectively on the Activities of Daily Vision Subscale. The authors concluded that the effect of dietary modification on the natural course of atrophic AMD warranted investigation in the context of a randomised, controlled trial.

Such an evaluation was conducted in the LAST (Lutein Antioxidant Supplementation Trial) study. Richer et al. 41 evaluated the effect of supplementation on visual performance in atrophic AMD on 90 subjects in a double blind, placebo controlled trial. Average MPOD increased by 0.09 log units (or 50 %) after 12 months, in the L and L plus antioxidant groups. The investigators observed concurrent and statistically significant improvements in contrast sensitivity, visual acuity and subjective measures of glare recovery in both treatment groups, but not in the control group. Snellen-equivalent acuity improved by 5.4 letters in patients supplemented with L, and by 3.5 letters in patients supplemented with L plus antioxidants, whereas improvements in contrast sensitivity were significantly better in the L plus antioxidant group than in the L group.

Falsini et al. 42 studied the effect of supplemental L on central retinal function, assessed electrophysiologically, in patients with early AMD, and reported a significant

Bartlett and Eperjesi 43 undertook a prospective, 9-month, double-masked randomised controlled trial of the effect of supplementation with lutein combined with vitamins and minerals on contrast sensitivity among participants with age related maculopathy and atrophic AMD. Contrast sensitivity was assessed using a Pelli-Robson chart and participants were randomised into active and placebo treatment groups. The authors report no significant improvement in contrast sensitivity among either group and suggest that supplementation with 6mg/L and other antioxidant vitamins and minerals has no tangible benefit to this group (although one could argue that preservation rather than enhancement of performance might be a more suitable outcome measure for AMD patients) and further, that determination of optimum dosage levels requires further work. Their findings are naturally confined to the somewhat limited measure of contrast sensitivity with a Pelli-Robson chart that may not be best equipped to detect subtle changes in performance. Failure to record MPOD at baseline, and the low dosage of supplemental L, represent design flaws in that study, and limit the scope for meaningful comment. Parisi et al. 44 have also recently explored the influence of short-term carotenoid and antioxidant supplementation on electrophysiologically assessed retinal function in early AMD. Of the 27 early AMD patients enrolled in their study, 15 had daily oral supplementation of vitamin C (180mg), vitamin E (30mg), zinc (22.5mg), copper (1mg), lutein (10mg), zeaxanthin (1mg), and astaxanthin (4mg) for 12 months, while the remaining 12 had no dietary supplementation during the same period. Fifteen age-similar healthy controls were also assessed at baseline and followed-up for the duration of the study period without supplementation. Multifocal electroretinograms, in response to 61 M-stimuli presented to the central 20 degrees of the visual field (averaged across 5 retinal eccentricity areas between the fovea and mid-periphery: 0 degrees to 2.5 degrees, 2.5 degrees to 5 degrees, 5 degrees to 10 degrees, 10 degrees to 15 degrees, and 15 degrees to 20 degrees) were assessed at baseline in controls and in early AMD patients, and again at 6 months and 12 months. At baseline, they observed highly significant reductions of N1-P1 response amplitude densities (RADs) for the central five degrees surrounding the fovea in AMD patients when compared with healthy controls. For more peripheral retinal eccentricities, RADs were not significantly different from controls. After 6 and 12 months of treatment, the treated group showed highly significant increases in N1-P1 RADs for the two most central retinal areas, but not for more peripheral eccentricities beyond 5 degrees. The non-treated control group exhibited no significant RAD changes at any eccentricity. These findings suggest that in early AMD eyes, central retinal function (0 degrees -5 degrees) can be improved by supplementation with carotenoids and co-antioxidants. The study design, however, does not clarify whether such improvements in retinal function have a measurable impact on visual performance and experience, and the failure to measure and record MPOD somewhat limits the interpretation of these potentially important findings.

Olmedilla et al. 45 investigated whether supplemental L influences visual function in patients with age-related cataract, where visual performance was evaluated by measures of visual acuity and glare sensitivity. This randomised, placebo-controlled trial revealed significant improvements in visual acuity and glare sensitivity following supplemental L, and the observed improvements were related to changes in serum levels of L, whereas no such improvements were observed in patients supplemented with placebo or with α-tocopherol. While contrast sensitivity was not recorded at baseline or during the supplementation phase, it is interesting to note that in cataract patients supplemented with lutein, contrast sensitivity at the end of the supplementation period was similar to or even better than that expected for control subjects of a similar age. The authors postulated that the observed improvements in the outcome measures were not the result of any change in the crystalline lens, but more likely to be the result of improved retinal function.

Photophobia is a phenomenon experienced by all persons when illumination is suddenly and dramatically changed from dark to light, and is typified by the experience of switching on a bedroom light at night time. However, under normal daylight conditions, the experience of photophobia is somewhat more variable. Numerous clinical conditions (e.g. RP & AMD) are associated with photophobia, and, even in the absence of detectable disease, clinicians are often presented with patients whose primary complaint is of periodic or persistent sensitivity to bright light (but at levels which do not similarly affect colleagues/friends/family). Given its absorption characteristics, the optical density of MP may be important in determining an individual's threshold for the subjective complaint of photophobia.

Stringham et al. 46 explored the effect of the spectral composition of a target on visual discomfort, using electromyography and a rating scale to determine photophobia thresholds. They showed that, while there was a positive relationship between wavelength and the energy needed to produce photophobia for wavelengths between 520 and 640nm, at shorter wavelengths there was a notch centred at 460nm, the trough and shape of which resembled the log transmittance spectrum of MP. Their findings led the authors to suggest that MP may attenuate photophobia or visual discomfort induced by short wavelength sources.

These observations prompted a subsequent study investigating the relationship, if any, between MP and photophobia. 47 This two-part experiment explored the relationship between baseline MPOD levels and photophobia thresholds, as well as the effect of augmenting MPOD on such thresholds. Four subjects were supplemented with 30mg/L and 2.7mg Z daily for 12 weeks. Peak MPOD was observed to increase from 0.452 (± 0.11) at baseline to 0.536 (± 0.11) at the end of the period of supplementation. A significant and inverse relationship between baseline MPOD and threshold for photophobia was observed, such that individuals with higher MPOD had higher tolerance for short wavelength light. Furthermore, increasing MPOD over a 12-week period appeared to increase the threshold for photophobia for all subjects for short wavelength sources.

Recently, Stringham & Hammond have explored the influence of glare on visual performance, and how MPOD might influence any observed relationships. They first looked at baseline visual performance under glare conditions by evaluating photostress recovery (a sensitive indicator of macular function) and grating visibility. 48 The effect of veiling glare on grating visibility was explored using a five cycles per degree contrast grating stimulus, surrounded by a concentric annulus of adjustable intensity. For the photostress recovery test, the same stimulus was viewed following photostress with a 5 degree xenon white disc providing 5.5 log Trolands of retinal illuminance over 5 seconds’ duration. MPOD was a significant determinant of the deleterious effects of glare, with visual thresholds and photostress recovery times significantly and inversely related to MPOD. Further, high MPOD was associated with better visual performance in a way that was consistent with its spectral absorbance and spatial profile.

These observations prompted the same investigators to design and execute a trial of supplemental L (10mg per day) and Z (2mg per day), using the same testing conditions, but on this occasion looking for changes in performance associated with augmentation of MPOD. In this instance, they found that, following six months of supplementation, and an average increase in MPOD from 0.41 to 0.57, most subjects exhibited improved photostress recovery and glare tolerance in association with an increase in MPOD. More specifically, a 39 % increase in MPOD enhanced tolerance of intense glaring light by up to 58 % and reduced photostress recovery times by 14 %. 49

Although the authors wisely suggest a cautionary approach to the interpretation of their data and the wider implications of such findings, their conclusion that the results are “both large enough and sufficiently general to be meaningful in real life”, and that “supplementing L and Z could indeed be palliative for those suffering the consequences of glare”, is important and warrants further investigation in the form of a randomised clinical trial.

Engles et al. 50 have investigated the “acuity hypothesis”, exploring the relationship between MPOD and gap acuity and vernier acuity under “photopic” conditions. They report that neither gap acuity nor vernier acuity were significantly related with MPOD, and concluded that their “data suggest that the predictions of the acuity hypothesis do not hold”. While the authors qualify their findings as appropriate to their specific testing conditions alone, several study limitations (other than those recognised by the authors) warrant brief discussion.

Firstly, although the authors report that their conclusions are relevant for photopic conditions, their adopted background luminance levels are in the low photopic range at best (17cd/m2 for the achromatic condition, and 15.7 cd/m2 for the chromatic condition), and certainly not appropriate for evaluation of photopic visual function. Indeed, given the subtle nature of any performance changes likely to be facilitated by MP, the background luminance difference (≈8 %) between the two testing conditions is also a potentially confounding factor.

Secondly, while all subjects were corrected to 6/6, it is plausible, indeed probable, that the actual acuity limits of their study population ranged widely between the 6/6 level employed up to a likely 6/3 limit for a young healthy subject. This potential two-fold range in acuity, subserved by individual optical, anatomic and neural architectures, would have a strong influence on both gap and vernier acuity tasks, almost certainly more powerful than MPOD. Also, by adopting a 6/6 limit, the investigators most likely failed to correct for potentially significant amounts of uncorrected axial astigmatism in some subjects, which could significantly influence performance on both of the chosen tasks (testing of vernier and gap acuity limits). While the authors could argue that any such variables remained consistent between testing conditions, we believe it would be more appropriate to eliminate sources of variability such as residual refractive error, so that all subjects operate at their limits of acuity.

The adoption of a single spatial frequency and contrast setting further limits the conclusions that can be drawn from this paper. The effect of MP, for example, might differ significantly under different spatial frequency and or contrast ranges. Assessment of visual performance across the full contrast sensitivity function might represent a more thorough and rigorous assessment of MP's capacity to affect visual performance through attenuation of the effects of chromatic aberration and light scatter.

Finally, the subjects employed in the Engles study typically exhibited average to high MP levels, with few subjects exhibiting MP levels below 0.20. Reading and Weale 15 previously modelled the potential effect on MP in terms of attenuation of the effects of chromatic aberration, and suggested that, due to the non-linear nature of the effect, MPOD levels above 0.30 were probably superfluous. Based on the assumptions of this model, a study on the effect of MP on visual performance might require the inclusion of relatively more subjects that exhibit low MPOD levels inorder to demonstrate an effect.

These limitations of the cited study serve to emphasize the challenges inherent in investigating the role of MP in visual performance and experience, which rest on the need (insofar as is possible) to disentangle the influence of MP from the often unquantifiable and variable influences of individual optical and neural architectures.

Loughman et al., 51 in a cross sectional analysis involving some 142 young healthy subjects, observed statistically significant relationships between MPOD and best corrected visual acuity, and also with photopic and mesopic contrast sensitivity at intermediate spatial frequencies. MP appeared to contribute to up to a 0.1 log unit refinement of high contrast visual acuity (equivalent to one extra line on the acuity chart, or the effective correction of up to 0.25D or residual blur). The correlations between MPOD and visual acuity and contrast sensitivity however, although statistically significant, account for only a small percentage of the potential variability (r2 values < 10 %), so should be interpreted cautiously with respect to its clinical relevance in the absence of a more rigorous placebo controlled supplementation study.

Bartlett and Eperjesi 52 set out to explore the effect of L supplementation on visual performance among healthy observers. Similar to their AMD trial (2007), the authors report no effect of supplementation on performance measures ranging from distance and near visual acuity, contrast sensitivity and photostress recovery. The results are somewhat unsurprising however given (a) the low dose, 6mg/L supplement used, (b) the basic nature of the series of tests employed to evaluate visual performance, and (c) the small number of subjects tracked over 9 months (n = 46) and 18 months (n = 29) across such a broad age range (22-73 years). Once again, their failure to record MPOD or serum L and Z levels means that only qualified comment can be made as to the significance of the reported findings.

Armstrong et al., in a primitively designed pilot study (involving only one subject) presented at a recent conference (ARVO 2008, Poster # 4964/D984), evaluated macular function on a serial basis throughout a 4-month period of supplementation with L and Z. Looking at a series of psychophysical and electrophysiological outcome measures, they evaluated the effect of supplementation on dark-adapted thresholds and recovery kinetics, pattern visual evoked potentials (PVEPs) [before and after photostress], and PERG amplitude. An MPOD increase of approximately 33 % was accompanied by a 23 % improvement in 650nm dark adapted thresholds (from 30dB to 37dB) and by an increase in PERG amplitude, but not by a change in cone recovery kinetics or photostress PVEP recovery. Although these findings should be interpreted with caution, particularly given that only one subject was tested, they are again suggestive of an improvement in macular function following augmentation of MPOD in young healthy subjects.

The inconsistencies in spatial vision data with respect to MPOD reflect the difficulty inherent in isolating performance tasks which may be influenced by MP. Furthermore, the wide inter-individual variability of MPOD 53 renders the interpretation of such studies all the more challenging, particularly where such investigations depend on cross-sectional rather than longitudinal data. It would however seem to be the case that, as far as spatial vision is concerned, the effect, if any, of MP on performance appears small, at least for individuals with average to high MPOD.

Since the MP absorption spectrum ranges from about 400 to 520nm and peaks at 460nm, 54 it would seem likely that these pigments influence colour vision through selective absorption of short wavelengths, thereby influencing the short-wave sensitive (SWS) cones and the blue-yellow opponent-colour channel. Moreland and Dain 55 (1995) reported that hue discrimination, measured using the Farnsworth-Munsell 100-Hue test (FM100), is indeed adversely affected (primarily) for blue wavelengths, by simulation of high MPOD using liquid notch filters containing carotene in a benzene solution. Comparing the results with those obtained with a neutral filter, they concluded that this effect was not simply the result of reduced retinal illuminance. Further evidence supporting an effect of MPOD on short wavelength vision has been obtained from studies of SWS cone sensitivity. 56,57 It has also been shown that colour discrimination measured by a colour matching technique is influenced by MPOD. 58,59

However, two recent studies using alternative methods, produced conclusions differing from those of the above mentioned studies. Firstly, a study of the effects of dietary supplementation with macular carotenoids on MP found no correlation between the level of MP (measured by heterochromatic flicker photometry) and red-green (RG) or yellow-blue (YB) colour discrimination thresholds, though it was reported that RG vision was improved following supplementation. 60 Secondly, RG cancellation profiles have been reported to be highly correlated with MPOD, while profiles for YB were independent of both eccentricity and MPOD. 61 Further support comes from a study of anomaloscope Moreland match midpoint data, in which no difference was reported between post-cataract patients with blue-absorbing intra-ocular lenses (IOLs) and those with clear IOLs. 62

Thus, the influence, if any, of MP on colour vision remains uncertain at the present time. However, It is possible that an artificial filter creates short-term changes in colour vision and that an autoregulatory process adjusts retinal and/or cortical colour mechanisms on a long-term basis in response to an individual's naturally occurring MPOD. 61 This hypothesis is supported by data showing a consistent shift in achromatic locus over a three month period for post-surgical cataract patients, 63 and by evidence of plasticity of adult neural colour mechanisms. 64

In the elderly, pre-retinal image degradation and slower encoding results in featurally-compromised representation of spatially-extended search arrays. Even with appropriate optical correction, older adults therefore do not possess the spatial resolving power of the young adult. Such losses are not confined to high spatial frequencies, but contrast sensitivity losses are observed across a range of intermediate frequencies. 65 Indeed, many changes in both structure and function of the visual system, such as pupillary miosis and loss of crystalline lens transparency, 66 accompany the aging process (summarised elsewhere 67). The consequence of such changes is a reduction in retinal illuminance, such that equiluminant stimuli do not result in equal retinal illuminance for different age groups. Human visual performance therefore tends to decrease with age (Figure 4). Such effects are to some extent unavoidable, and a natural consequence of aging.

Figure 4.

Effect of normal aging on contrast sensitivity. Experimental data show a 1-log unit sensitivity decrease from age 60 to 95.

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Reprinted with permission: Haegerstrom-Portnoy, et al. 2007;79.

The most significant role of MP in vision, however, may rest on the potential of L, Z and meso-Z to retard the aging process through their antioxidant properties. It is important to note that MP acts, uniquely, as an antioxidant, both passively and actively, the former mechanisms being dependent on its ability to limit photo-oxidative damage by filtering short wavelength light at a pre-receptorial level and the latter mechanism attributable to its capacity to quench reactive oxygen intermediates.

The inter-individual variability in MPOD, consistently observed in cross-sectional studies, may have important implications for the long term health and viability of the central retina. In subjects with little MP, the cumulative and chronic effects of increased exposure of photoreceptors to short wavelength light, coupled with a weaker local capacity to quench free radicals, could, in theory at least, accelerate the onset of physiological and pathological aging of the retina.

In support of such a notion, Hammond et al. 56 have shown that high MPOD was associated with the retention of youthful scotopic and short wave sensitivity and suggested that MP may retard an age-related visual decline. The potential benefits of increased MPOD appear not to be confined to the retina. Hammond et al. 68 reported a positive and significant association between crystalline lens transparency and MPOD, and speculated that high concentrations of the macular carotenoids in the lens probably accompany high concentrations at the macula, and protect against the effects of oxidation in the lens (thereby maintaining transparency). Indeed, other studies have shown an association between a high dietary intake of L and Z with decreased incidence of cataract formation. 69,70

Werner and Steele 71 demonstrated age-related sensitivity losses of foveal colour mechanisms across all three cone types, although the sensitivity loss for short wavelength sensitive cones (S-cone) was lower (at 0.08 log units per decade), when compared to 0.11 log units loss per decade for both medium (M-cone) and long wave (L-cone) cones. Werner et al. 57 later explored the senescence of foveal and parafoveal cone sensitivities and their relation to MPOD. Again, they report age-related decline of foveal and parafoveal increment thresholds. Interestingly however, and consistent with the hypothesis that the MP protects the photoreceptors from senescent losses in sensitivity, a significant and positive correlation was found between foveal MPOD and differential S-cone log sensitivity losses at the fovea and at the parafovea, but not with differential M- and L- cone log sensitivity losses at the retinal loci. This finding, however, was independent of age, prompting the authors to postulate that it was due to local gain changes, resulting from differential filtering of incident light by the MP between the fovea and the parafovea.

Haegerstrom-Portnoy 72 also examined S-cone versus L-cone sensitivity in a group of young and older adults to determine whether MP protects the human fovea from retinal neural damage caused by visible-light exposure over a lifetime. While there was no difference observed for L-cone sensitivity between groups, the older group showed a significant differential loss of S-cone sensitivity across the retina compared with the younger group, with greater loss of sensitivity at non-foveal locations than at the fovea. This observation is again suggestive of a protective effect of MP on foveal function.

Schupp et al. 73 endeavored to explore the hypothesis from a different perspective, postulating that if high levels of MP might forestall the effects of normal aging, then low levels of MP might accelerate the normal aging process. Cystic fibrosis (CF) is a condition associated with defective gastrointestinal absorption of carotenoids as a result of pancreatic insufficiency. Low serum concentrations of carotenoids, including the constituents of MP, are invariably reported in CF patients. Given the repeatedly observed positive and significant relationship between MPOD and serum concentrations of its constituent carotenoids (reviewed elsewhere 74), it can be reasoned that patients with CF would have low MPOD. Schupp et al. 73 assessed visual performance in ten cystic fibrosis patients, in whom serum concentrations of L and Z and MPOD were predictably and significantly lower than control subjects, and typically less than 50 % of the values observed amongst control subjects. However, visual performance (contrast sensitivity, colour discrimination and multifocal ERG amplitudes) were statistically similar for CF patients and control subjects.

While the basic rationale of this study is provocative, there are however a number of concerns with the methodology. With six of the ten CF subjects aged between 21-27 years, it is unlikely that such a youthful population sample would demonstrate accelerated aging effects on visual function (even in the presence of chronically low MPOD levels). In any case, given the theoretical possibility that higher levels of MP might be associated with enhanced visual performance, it is unclear from this publication as to how functional differences, which might have been observed between the CF and control groups, could be attributable to age effects rather than simply to differences in MPOD. The authors conceded that a longitudinal assessment of an older CF population is required to address the hypothesis more appropriately.

Hammond and Wooten 75 investigated the relationship between MP, critical flicker fusion frequency (CFF) and age, citing CFF as a general measure of visual health. They found a significant decline in CFF values with age. There was a significant and positive relationship however between MPOD and CFF values that was independent of age. The authors conclude that these results are consistent with a protective effect of MP on visual health across the lifespan. While such investigations appear to be at a very early stage, preliminary results suggest a role for MP in temporal vision and, specifically, that high MPOD may protect the retina and defer some typical age-related changes in temporal vision.