«Wild Edible Plant Consumption and Age-Related Cataracts in a Rural Lebanese Elderly Population: A Case control Study By Joelle Zeitouny School of ...»
It is estimated that macular pigments reduce the blue light intensity normally by 40% (Landrum et al., 1997). However, if sufficiently dense, they only allow 10% of 460nm light (Figure 2.8) to reach the vulnerable outer segments of the foveal cones (Wyszecki & Stiles, 1982).
Figure 2.8: Macular pigment optical density and light transmission.
A double Y plot showing subjects with high v/s low macular pigment (left ordinate) plotted against (right ordinate) the relative energy of midday sunlight (correlated color temperature of 6500°K) derived from tabular data provided in Wyszecki and Stiles (1982), (Hammond et al., 2001).
In the outer retina, oxygen partial pressure is so high that it results in a high rate of blue light-induced singlet oxygen formation (Schmidt-Erfurth, 2005). In fact, 14 one of the ways light damages the retina is by generation of free radicals that lead to peroxidation of membrane lipids (Johnson, 2002). Direct oxidation products of lutein and zeaxanthin have been reported there, indicating that these carotenoids do act as antioxidants in the macula (Khachik et al., 1997). Actually, it is hypothesized that lutein and zeaxanthin are able to quench free radicals and to react with the peroxy radicals that are involved with lipid peroxidation (Landrum & Bone, 2001). The inhibition of lipid peroxidation is desirable in the retina because of the high concentration of polyunsaturated fatty acids in the photoreceptor membranes (Beatty et al., 2000). On the other side of the coin, lutein may also prevent cellular damage in certain forms of cardiovascular disease (Dwyer et al., 2001), stroke (Ascherio et al., 1999), and cancer (Bidoli et al., 2003) by quenching singlet oxygen or neutralizing photosensitizers.
Lutein and zeaxanthin do not protect only the retina from oxidative damage.
They also protect the lens since, within the lens, around 74% of lutein and zeaxanthin are located between the epithelium and the cortex, area where oxygen might be expected to stress the lens the most strongly (Yeum et al., 1999).Thus, these antioxidant pigments may help prevent oxidation of epithelial lipids, which is an important etiological factor in cataract development (Bhuyan & Bhuyan, 1984). In fact, in 2004, Chitchumroonchokchai et al. provided the first data demonstrating that lutein and zeaxanthin decrease UVB-induced lipid peroxidation and attenuate the activation of the stress signaling pathways in human lens epithelial cells. TrevithickSutton et al. (2006) decided to further investigate the possibility that lutein and zeaxanthin exerted their protective effect by scavenging free radicals by examining their effect on superoxide and hydroxyl radicals. Both lutein and zeaxanthin scavenged the hydroxyl radicals more effectively than superoxide radicals, zeaxanthin being the most powerful hydroxyl radical scavenger. The mechanism of hydroxyl radical scavenging could occur, according to Trevithick-Sutton et al. (2006), via bond formation between the hydroxyl radical and one of the double bonds in lutein and zeaxanthin. Lutein, containing only 10 conjugated double bonds, compared to the 11
2.4.4 Body of evidence to support a protective role for lutein and zeaxanthin in two common eye diseases of aging, cataract and macular degeneration 22.214.171.124 Lutein and zeaxanthin and age-related cataracts Age-related cataracts are the most common type of cataracts. Cataracts are ocular opacities, partial or complete in one or both eyes, on or within the lens. They are divided into three subtypes based on location (nuclear, cortical and posterior subcapsular). These opacities are caused by precipitation of oxidatively damaged proteins in the lens of the eye, often resulting in impaired vision or blindness (Bron et al., 2000).
Age is the most significant risk factor for late-onset cataract and the relationship between aging and lens optical density has been studied extensively (Coren & Girgus, 1972; Pokorny et al., 1987; Sample et al., 1988; Hammond et al., 1997). Smoking (DeBlack, 2003), diabetes (Klein et al., 1998; Saxena et al., 2004;
Hennis et al., 2004) and UV light exposure (McCarty & Taylor, 2002) have all also consistently been found to be associated with age-related cataracts. Dark iris color alters the effect of UV radiation that reaches the eye (possibly by raising the temperature of the lens and thus increasing molecular degradation and age-associated increases in lens optical density) and thus was found too to be directly related to agerelated cataracts (Hammond et al., 2000).
On the other hand, body mass index seems to be related in a U-shaped manner to age-related cataracts even though the nature of the relationship between body mass index and age-related cataracts has not been fully elucidated yet (Klein et al., 1998;
Jacques et al., 2003; Glynn et al., 1995; Weintraub et al., 2002; Hiller et al., 1998).
Women seem to have higher rates of cataract across racial groups, even when adjusting for women’s greater longevity, probably because, by nature, they have more
Finally, studies examining the association between age-related cataracts and myopia (McCarty et al., 1999; Mukesh et al., 2006), corticosteroids use (Carnahan & Goldstein, 2000; Toogood et al., 1993), exogenous estrogen use (Mukesh et al., 2006;
Younan et al., 2002) and genetics (Sekine et al., 1995; Alberti et al., 1996; Okano et al., 2001; Maraini et al., 2003) have yielded conflicting results.
Experimental studies in vivo
Many experimental animals do have lenses but since the levels of lutein and zeaxanthin in the lenses of these animals are not known, and since there is no evidence that dietary lutein or zeaxanthin influence the levels of these carotenoids in the lenses of those experimental animals, there were no studies on cataracts in experimental animals (Mares-Perlman et al., 2002). The only experimental evidence that lens carotenoids in adult vertebrates can be manipulated by dietary supplements was provided two years ago by Dorey et al. (2005). Quails fed with a diet supplemented with a high dose of zeaxanthin had significantly higher lens zeaxanthin than quails fed with a diet with no or a lower dose of zeaxanthin (p 0.0001).
Unfortunately, the study did not examine the impact of supplementing the diet with lutein on lens carotenoids and lens lutein was not affected by dietary supplementation with zeaxanthin (p ≥ 0.18).
Epidemiological evidence A few studies have specifically examined the relationship between lutein and zeaxanthin and cataract risk. Chasan-Taber et al. (1999) noted that US women who 17 had the highest intake of lutein and zeaxanthin had a 22% decreased risk of cataract extraction compared with those in the lowest quintile (RR: 0.78; 95% CI: 0.63, 0.95;
p- trend = 0.04). In men with higher intakes of lutein and zeaxanthin but not of other carotenoids, Brown et al. (1999) also noted that there was a lower risk of cataract extraction: men in the highest fifth of lutein and zeaxanthin intake had a 19% lower risk of cataract relative to men in the lowest fifth (RR: 0.81; 95% CI: 0.65–1.01; ptrend=0.03).
Moreover, in 1995, a retrospective study by Mares-Perlman et al. of 1919 participants in the Beaver Dam Study, found that women in the highest quintile category of lutein intake ten years prior to study enrollment (median 949 µg/day) had a 27% lower prevalence of cataracts (OR: 0.73; 95% CI: 0.5–1.06; p-trend=0.02) than women in the lowest quintile category of lutein intake (median 179 µg/day). Of the lutein-rich foods examined, only spinach was found to be inversely associated with cataract formation.
In 1999, after five years of follow-up, Lyle et al. (1999a) found that members of the Beaver Dam cohort who were in the highest quintile category of lutein intake 10 years before baseline (median 1,245 µg/1000 kcal) were 50% less likely to develop nuclear cataracts (RR: 0.5; 95% CI: 0.3–0.8; p-trend=0.002) than those in the lowest quintile category of intake (median 298 µg/1000 kcal). As in the first study, consumption of spinach and other dark leafy greens at baseline was inversely associated with risk of nuclear cataract. In addition, an inverse association between serum lutein concentrations and risk of nuclear cataract was observed in people aged more than 65 years (OR: 0.3; 95% CI: 0.1–1.2; p-trend=0.15), although this association was not statistically significant (Lyle et al., 1999b).
As a matter of fact, the Melbourne Visual Impairment Project, an Australian population-based prevalence study of eye disease that included both residential and nursing home populations, found that nuclear cataract was the only type of cataract to be significantly associated with dietary intake of lutein and zeaxanthin (Vu et al., 18 2006). An inverse association was observed between high dietary intake of lutein and zeaxanthin and the prevalence of nuclear cataract (OR: 0.58; 95% CI: 0.37-0.92; ptrend = 0.023 and OR: 0.64; 95% CI: 0.40-1.03; p-trend =0.018 for those in the top quintile of crude and energy-adjusted lutein and zeaxanthin intake, respectively).
Bearing this in mind, Gale et al. had found in 2001 that, after adjustment for age, gender, and other risk factors, the risk of nuclear cataract was lowest in people with the highest plasma concentrations of α-carotene (OR: 0.5; 95% CI: 0.3-0.9; p-trend = 0.006) or β-carotene (OR: 0.7; 95% CI: 0.4-1.4, p-trend = 0.033). Plasma concentrations of lutein were only significantly associated with a lower risk of posterior subcapsular cataract (OR: 0.5; 95% CI: 0.2-1.0; p-trend = 0.012) and plasma concentrations of zeaxanthin did not seem to be inversely associated with any type of cataract.
On the other hand, a prospective analysis of the Nurses Health Study cohort reported that the rate of cataract surgery was associated with lower intakes of luteinrich foods such as spinach and other green vegetables (Hankinson et al., 1992).
Consumption of spinach and other greens at least five times per week compared to less than once a month resulted in a 47% lower risk for cataract extraction during up to eight years of follow-up (RR: 0.53; 95% CI 0.38–0.73; p-trend=0.001).
In a double-blind study involving dietary supplementation with lutein (15 mg/d, 3 times/wk for up to 2 years, n = 5), α-tocopherol (100 mg/d, 3 times/wk (n =
6) or placebo (n = 6) in patients with cataracts, visual performance (visual acuity and glare sensitivity) improved in the lutein supplemented group only (Olmedilla et al., 2003). As a matter of fact, a recent study reported that a high dose combination of antioxidants (vitamins C and E, β-carotene, and zinc) had no significant effect in the development or progression of cataract (Age-Related Eye Disease Study Research Group, 2001b). Similarly, The Roche European–American Anticataract Trial (REACT), a randomized placebo-controlled 3-year trial, concluded that a mixture of oral antioxidant micronutrients (b-carotene, 18 mg/d; vitamin C, 750 mg/d; vitamin E, 19 600 mg/d) only produced a small deceleration in progression of age-related cataract (Chylak et al., 2002).
These studies suggest, despite differences in study design, case definition and exposure measurement, that dietary lutein and zeaxanthin play a role in cataract prevention and that spinach and other dark leafy greens, the most concentrated sources of dietary lutein and zeaxanthin, are most consistently associated with protection against cataract.
126.96.36.199 Lutein and zeaxanthin and age-related macular degeneration
Age-related macular degeneration is the principal cause of blindness in the elderly population in the USA and the Western world (Mozaffarieh et al., 2003). It is a degradation of the central portion of the retina which includes the macula. There are two types of age-related macular degeneration: “wet” (or neovascular) and “dry” (or atrophic) (The Macular Degeneration Partnership, 2007). It is possible to experience both types at the same time, in one or both eyes. In “wet” age-related macular degeneration, tiny unhealthy blood vessels grow under the retina and often break and leak, causing loss of vision. Conversely, in “dry” age-related macular degeneration, the most common type, there is a breakdown or thinning in the macula of the retinal pigment epithelial cells (RPE) which are light sensitive and contain hundreds of photoreceptors. The death or degeneration of these cells is called atrophy (hence, the name atrophic age-related macular degeneration) and reduces one's central vision and can affect color perception. Generally, the damage caused by the “dry” form is not as severe or rapid as that of the “wet” form but can, over time, cause profound vision loss.
Aside from age (McCarty et al., 2001) and family history (Silvestri et al., 1994; Heiba et al., 1994; Klein et al., 2001b), smoking (McCarty et al., 2001;
Thornton et al., 2005) has been the most consistent factor associated with the prevalence and, to a lesser extent, the incidence of age-related macular degeneration.
20 High body mass index was also positively associated with age-related macular degeneration (Klein et al., 2001a) but, oddly enough, the latter was inversely related to blood lipid levels (Hyman et al., 2000; Klein et al., 2003a). In fact, persons with low serum high-density lipoprotein (HDL) cholesterol or high low-density lipoprotein (LDL) cholesterol were more likely to have a lower prevalence and incidence of agerelated macular degeneration (according to Malek et al. (2003), because of the downregulation of LDL receptors that occurs in the retinal pigment epithelium, subsequent to high plasma cholesterol). Nonetheless, there are neither epidemiologic nor clinical trial data showing an association of lipid-lowering with a reduction in risk of age-related macular degeneration.
On the other hand, observational studies linking age-related macular degeneration to systemic hypertension (Hyman et al., 2000; Klein et al., 1993; The Eye Disease Case Control Study Group, 1992), atherosclerosis (Vingerling et al., 1995a; Klein et al., 1993), exogenous estrogen use (The Eye Disease Case Control Study Group, 1992; Klein et al., 1994), statin use (McGwin et al., 2003; Klein et al., 2003b), gender (Vingerling et al., 1995b; Klein et al., 1992), UV light exposure (Klein et al., 1993; The Eye Disease Case Control Study Group, 1992) and iris color (Hammond et al., 1996; Nicolas et al., 2003; Khan et al., 2006) have given conflicting results.
Experimental studies in vivo and in vitro